Publications by authors named "Patricia L Mitchell"

27 Publications

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Reply to: "Dietary sucrose induces atherosclerotic diseases more than dietary fat in LDLrApoB mice: Is it independent of differences in plasma cholesterol levels?"

Atherosclerosis 2021 Apr 5. Epub 2021 Apr 5.

Quebec Heart and Lung Institute, Department of Medicine, Faculty of Medicine, Laval University, Quebec City, Quebec, Canada; Institute of Nutraceuticals and Functional Foods, Laval University, Quebec City, Quebec, Canada. Electronic address:

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http://dx.doi.org/10.1016/j.atherosclerosis.2021.03.038DOI Listing
April 2021

Cholecalciferol Supplementation Does Not Prevent the Development of Metabolic Syndrome or Enhance the Beneficial Effects of Omega-3 Fatty Acids in Obese Mice.

J Nutr 2021 Apr 13. Epub 2021 Apr 13.

Québec Heart and Lung Institute Research Centre, Faculty of Medicine, Laval University, Québec City, QC, Canada.

Background: Cholecalciferol (D3) may improve inflammation, and thus provide protection from cardiometabolic diseases (CMD), although controversy remains. Omega-3 fatty acids (ω-3FA) may also prevent the development of CMD, but the combined effects of ω-3FA and D3 are not fully understood.

Objectives: We determined the chronic independent and combined effects of D3 and ω-3FA on body weight, glucose homeostasis, and markers of inflammation in obese mice.

Methods: We gave 8-week-old male C57BL/6J mice, which had been fed a high-fat, high-sucrose (HF) diet (65.5% kcal fat, 19.8% kcal carbohydrate, and 14% kcal protein) for 12 weeks, either a standard D3 dose (+SD3; 1400 IU D3/kg diet) or a high D3 dose (+HD3; 15,000 IU D3/kg diet). We fed 1 +SD3 group and 1 +HD3 group with 4.36% (w/w) fish oil (+ω-3FA; 44% eicosapentaenoic acid, 25% docosahexaenoic acid), and fed the other 2 groups with corn oil [+omega-6 fatty acids (ω-6FA)]. A fifth group was fed a low-fat (LF; 15.5% kcal) diet. LF and HF+ω-6+SD3 differences were tested by a Student's t-test and HF treatment differences were tested by a 2-way ANOVA.

Results: D3 supplementation in the +HD3 groups did not significantly increase plasma total 25-hydroxyvitamin D and 25-hydroxyvitamin D3 [25(OH)D3] versus the +SD3 groups, but it increased 3-epi-25-hydroxyvitamin D3 levels by 3.4 ng/mL in the HF+ω-6+HD3 group and 4.0 ng/mL in the HF+ω-3+HD3 group, representing 30% and 70%, respectively, of the total 25(OH)D3 increase. Energy expenditure increased in those mice fed diets +ω-3FA, by 3.9% in the HF+ω-3+SD3 group and 7.4% in the HF+ω-3+HD3 group, but it did not translate into lower body weight. The glucose tolerance curves of the HF+ω-3+SD3 and HF+ω-3+HD3 groups were improved by 11% and 17%, respectively, as compared to the respective +ω-6FA groups. D3 supplementation, within the ω-3FA groups, altered the gut microbiota by increasing the abundance of S24-7 and Lachnospiraceae taxa compared to the standard dose, while within the ω-6FA groups, D3 supplementation did not modulate specific taxa.

Conclusions: Overall, D3 supplementation does not prevent CMD or enhance the beneficial effects of ω-3FA in vitamin D-sufficient obese mice.
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http://dx.doi.org/10.1093/jn/nxab002DOI Listing
April 2021

Fish oil replacement prevents, while docosahexaenoic acid-derived protectin DX mitigates end-stage-renal-disease in atherosclerotic diabetic mice.

FASEB J 2021 May;35(5):e21559

Quebec Heart and Lung Institute, Laval University, Quebec, QC, Canada.

Diabetic nephropathy (DN) remains the major cause of end-stage renal disease (ESRD). We used high-fat/high-sucrose (HFHS)-fed LDLr /ApoB mice with transgenic overexpression of IGFII in pancreatic β-cells (LRKOB100/IGFII) as a model of ESRD to test whether dietary long chain omega-3 polyunsaturated fatty acids LCω3FA-rich fish oil (FO) could prevent ESRD development. We further evaluated the potential of docosahexaenoic acid (DHA)-derived pro-resolving lipid mediators, 17-hydroxy-DHA (17-HDHA) and Protectin DX (PDX), to reverse established ESRD damage. HFHS-fed vehicle-treated LRKOB100/IGFII mice developed severe kidney dysfunction leading to ESRD, as revealed by advanced glomerular fibrosis and mesangial expansion along with reduced percent survival. The kidney failure outcome was associated with cardiac dysfunction, revealed by reduced heart rate and prolonged diastolic and systolic time. Dietary FO prevented kidney damage, lean mass loss, cardiac dysfunction, and death. 17-HDHA reduced podocyte foot process effacement while PDX treatment alleviated kidney fibrosis and mesangial expansion as compared to vehicle treatment. Only PDX therapy was effective at preserving the heart function and survival rate. These results show that dietary LCω3FA intake can prevent ESRD and cardiac dysfunction in LRKOB100/IGFII diabetic mice. Our data further reveals that PDX can protect against renal failure and cardiac dysfunction, offering a potential new therapeutic strategy against ESRD.
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http://dx.doi.org/10.1096/fj.202100073RDOI Listing
May 2021

Circulating galectin-3 levels are not associated with non-alcoholic fatty liver disease: A Mendelian randomization study.

J Clin Endocrinol Metab 2021 Mar 8. Epub 2021 Mar 8.

Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec, Canada.

Context: The impact of galectin-3 inhibitors on non-alcoholic fatty liver diseases (NAFLD)-related outcomes is currently under investigation in randomized clinical trials. Whether there is a causal association between plasma galectin-3 levels and NAFLD is unknown.

Objective: To evaluate the causal effect of circulating galectin-3 levels on NAFLD as well as >800 other human diseases.

Design: Inverse variance weighted Mendelian randomization (IVW-MR) and phenome-wide MR.

Setting: Summary statistics of genome-wide association studies.

Patients: Participants of the UK Biobank, eMERGE, FinnGen, PREVEND and IMPROVE cohorts.

Intervention: Identification of independent single-nucleotide polymorphisms (SNPs) associated with galectin-3 levels (p<5x10 -8) in the PREVEND (14 SNPs) and IMPROVE (3 SNPs) cohorts.Main outcome measures: Presence of NAFLD in a meta-analysis of genome-wide association study of the eMERGE, UK Biobank and FinnGen cohorts (3042 NAFLD cases and 504,853 controls), as well as >800 other human diseases in the UK Biobank and FinnGen.

Results: Using IVW-MR, we found no causal association between galectin-3 levels and NAFLD in the meta-analysis of the 3 cohorts or in each individual cohort. After correction for multiple testing, we found no causal association between galectin-3 levels and >800 human disease-related traits.

Conclusions: This MR study revealed no causal associations between circulating galectin-3 levels and NAFLD or any other disease traits, suggesting that plasma galectin-3 levels may not be directly implicated in the pathogenesis of NAFLD or other human diseases.
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http://dx.doi.org/10.1210/clinem/dgab144DOI Listing
March 2021

High-Fat Diet Modulates Hepatic Amyloid β and Cerebrosterol Metabolism in the Triple Transgenic Mouse Model of Alzheimer's Disease.

Hepatol Commun 2021 Mar 18;5(3):446-460. Epub 2020 Dec 18.

Axe Neurosciences Centre De Recherche du CHU de Québec-Université Laval Québec Canada.

Obesity and diabetes are strongly associated not only with fatty liver but also cognitive dysfunction. Moreover, their presence, particularly in midlife, is recognized as a risk factor for Alzheimer's disease (AD). AD, the most common cause of dementia, is increasingly considered as a metabolic disease, although underlying pathogenic mechanisms remain unclear. The liver plays a major role in maintaining glucose and lipid homeostasis, as well as in clearing the AD neuropathogenic factor amyloid-β (Aβ) and in metabolizing cerebrosterol, a cerebral-derived oxysterol proposed as an AD biomarker. We hypothesized that liver impairment induced by obesity contributes to AD pathogenesis. We show that the AD triple transgenic mouse model (3xTg-AD) fed a chow diet presents a hepatic phenotype similar to nontransgenic controls (NTg) at 15 months of age. A high-fat diet (HFD), started at the age of 6 months and continued for 9 months, until sacrifice, induced hepatic steatosis in NTg, but not in 3xTg-AD mice, whereas HFD did not induce changes in hepatic fatty acid oxidation, lipogenesis, and gluconeogenesis. HFD-induced obesity was associated with a reduction of insulin-degrading enzyme, one of the main hepatic enzymes responsible for Aβ clearance. The hepatic rate of cerebrosterol glucuronidation was lower in obese 3xTg-AD than in nonobese controls ( < 0.05) and higher compared with obese NTg ( < 0.05), although circulating levels remained unchanged. Modulation of hepatic lipids, Aβ, and cerebrosterol metabolism in obese 3xTg-AD mice differs from control mice. This study sheds light on the liver-brain axis, showing that the chronic presence of NAFLD and changes in liver function affect peripheral AD features and should be considered during development of biomarkers or AD therapeutic targets.
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http://dx.doi.org/10.1002/hep4.1609DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7917280PMC
March 2021

Interaction of Autotaxin With Lipoprotein(a) in Patients With Calcific Aortic Valve Stenosis.

JACC Basic Transl Sci 2020 Sep 26;5(9):888-897. Epub 2020 Aug 26.

Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, Quebec, Canada.

Our objectives were to determine whether autotaxin (ATX) is transported by lipoprotein(a) [Lp(a)] in human plasma and if could be used as a biomarker of calcific aortic valve stenosis (CAVS). We first found that ATX activity was higher in Lp(a) compared to low-density lipoprotein fractions in isolated fractions of 10 healthy participants. We developed a specific assay to measure ATX-Lp(a) in 88 patients with CAVS and 144 controls without CAVS. In a multivariable model corrected for CAVS risk factors, ATX-Lp(a) was associated with CAVS (p = 0.003). We concluded that ATX is preferentially transported by Lp(a) and might represent a novel biomarker for CAVS.
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http://dx.doi.org/10.1016/j.jacbts.2020.06.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7524777PMC
September 2020

Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLrApoB mice.

Atherosclerosis 2020 07 24;304:9-21. Epub 2020 May 24.

Quebec Heart and Lung Institute, Department of Medicine, Faculty of Medicine, Laval University, Quebec City, Quebec, Canada; Institute of Nutraceuticals and Functional Foods, Laval University, Quebec City, Quebec, Canada. Electronic address:

Background And Aims: Poor dietary habits contribute to the obesity pandemic and related cardiovascular diseases but the respective impact of high saturated fat versus added sugar consumption remains debated. Herein, we aimed to disentangle the individual role of dietary fat versus sugar in cardiometabolic disease progression.

Methods: We fed pro-atherogenic LDLrApoB mice either a low-fat/high-sucrose (LFHS) or a high-fat/low-sucrose (HFLS) diet for 24 weeks. Weekly body weight gain was registered. 16S rRNA gene-based gut microbial analysis was performed to investigate gut microbial modulations. Intraperitoneal insulin (ipITT) and oral glucose tolerance test (oGTT) were conducted to assess glucose homeostasis and insulin sensitivity. Cytokines were assessed in fasted plasma, epididymal white adipose tissue and liver lysates. Heart function was evaluated by echocardiography. Aortic atheroma lesions were quantified according to the en face technique.

Results: HFLS feeding increased obesity, insulin resistance and dyslipidemia compared to LFHS feeding. Conversely, high sucrose consumption decreased gut microbial diversity while augmenting inflammation and the adaptative immune defense against metabolic endotoxemia and reduced macrophage cholesterol efflux capacity. This led to more severe cardiovascular complications as revealed by remarkably high level of atherosclerotic lesions and the early development of cardiac dysfunction in LFHS vs HFLS fed mice.

Conclusions: We uncoupled obesity-associated insulin resistance from cardiovascular diseases and provided novel evidence that dietary sucrose, not fat, is the main driver of metabolic inflammation accelerating severe atherosclerosis in hyperlipidemic mice.
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http://dx.doi.org/10.1016/j.atherosclerosis.2020.05.002DOI Listing
July 2020

The Hepatokine TSK does not affect brown fat thermogenic capacity, body weight gain, and glucose homeostasis.

Mol Metab 2019 12 4;30:184-191. Epub 2019 Oct 4.

Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec - Université Laval (CRIUCPQ), Québec City, Québec, Canada; Département de Médecine de l'Université Laval, Université Laval, Québec City, Québec, Canada; Centre de Recherche sur le Cancer de l'Université Laval, Université Laval, Québec City, Québec, Canada. Electronic address:

Objectives: Hepatokines are proteins secreted by the liver that impact the functions of the liver and various tissues through autocrine, paracrine, and endocrine signaling. Recently, Tsukushi (TSK) was identified as a new hepatokine that is induced by obesity and cold exposure. It was proposed that TSK controls sympathetic innervation and thermogenesis in brown adipose tissue (BAT) and that loss of TSK protects against diet-induced obesity and improves glucose homeostasis. Here we report the impact of deleting and/or overexpressing TSK on BAT thermogenic capacity, body weight regulation, and glucose homeostasis.

Methods: We measured the expression of thermogenic genes and markers of BAT innervation and activation in TSK-null and TSK-overexpressing mice. Body weight, body temperature, and parameters of glucose homeostasis were also assessed in the context of TSK loss and overexpression.

Results: The loss of TSK did not affect the thermogenic activation of BAT. We found that TSK-null mice were not protected against the development of obesity and did not show improvement in glucose tolerance. The overexpression of TSK also failed to modulate thermogenesis, body weight gain, and glucose homeostasis in mice.

Conclusions: TSK is not a significant regulator of BAT thermogenesis and is unlikely to represent an effective target to prevent obesity and improve glucose homeostasis.
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http://dx.doi.org/10.1016/j.molmet.2019.09.014DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889588PMC
December 2019

Maternal folic acid supplementation does not counteract the deleterious impact of prenatal exposure to environmental pollutants on lipid homeostasis in male rat descendants.

J Dev Orig Health Dis 2019 Sep 16:1-11. Epub 2019 Sep 16.

School of Nutrition, Faculty of Agricultural and Food Sciences, Centre de recherche en reproduction, développement et santé intergénérationnelle, Université Laval, Quebec City, QC, Canada.

Prenatal exposure to persistent organic pollutants (POPs) has been associated with the development of metabolic syndrome-related diseases in offspring. According to epidemiological studies, father's transmission of environmental effects in addition to mother's can influence offspring health. Moreover, maternal prenatal dietary folic acid (FA) may beneficially impact offspring health. The objective is to investigate whether prenatal FA supplementation can overcome the deleterious effects of prenatal exposure to POPs on lipid homeostasis and inflammation in three generations of male rat descendants through the paternal lineage. Female Sprague-Dawley rats (F0) were exposed to a POPs mixture (or corn oil) +/- FA supplementation for 9 weeks before and during gestation. F1 and F2 males were mated with untreated females. Plasma and hepatic lipids were measured in F1, F2, and F3 males after 12-h fast. Gene expression of inflammatory cytokines was determined by qPCR in epididymal adipose tissue. In F1 males, prenatal POPs exposure increased plasma lipids at 14 weeks old and hepatic lipids at 28 weeks old and prenatal FA supplementation decreased plasma total cholesterol at 14 weeks old. Prenatal POPs exposure decreased plasma triglycerides at 14 weeks old in F2 males. No change was observed in inflammatory markers. Our results show an impact of the paternal lineage on lipid homeostasis in rats up to the F2 male generation. FA supplementation of the F0 diet, regardless of POPs exposure, lowered plasma cholesterol in F1 males but failed to attenuate the deleterious effects of prenatal POPs exposure on plasma and hepatic lipids in F1 males.
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http://dx.doi.org/10.1017/S2040174419000497DOI Listing
September 2019

The hepatokine Tsukushi is released in response to NAFLD and impacts cholesterol homeostasis.

JCI Insight 2019 08 8;4(15). Epub 2019 Aug 8.

Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec - Université Laval (CRIUCPQ), Québec City, Québec, Canada.

Nonalcoholic fatty liver disease (NAFLD) prevails in obesity and is linked to several health complications including dyslipidemia and atherosclerosis. How exactly NAFLD induces atherogenic dyslipidemia to promote cardiovascular diseases is still elusive. Here, we identify Tsukushi (TSK) as a hepatokine induced in response to NAFLD. We show that both endoplasmic reticulum stress and inflammation promote the expression and release of TSK in mice. In humans, hepatic TSK expression is also associated with steatosis, and its circulating levels are markedly increased in patients suffering from acetaminophen-induced acute liver failure (ALF), a condition linked to severe hepatic inflammation. In these patients, elevated blood TSK levels were associated with decreased transplant-free survival at hospital discharge, suggesting that TSK could have a prognostic significance. Gain- and loss-of-function studies in mice revealed that TSK impacts systemic cholesterol homeostasis. TSK reduces circulating HDL cholesterol, lowers cholesterol efflux capacity, and decreases cholesterol-to-bile acid conversion in the liver. Our data identify the hepatokine TSK as a blood biomarker of liver stress that could link NAFLD to the development of atherogenic dyslipidemia and atherosclerosis.
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http://dx.doi.org/10.1172/jci.insight.129492DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6693835PMC
August 2019

Acute and chronic effect of bariatric surgery on circulating autotaxin levels.

Physiol Rep 2019 03;7(5):e14004

Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec, Québec, Canada.

Autotaxin (ATX), an adipose tissue-derived lysophospholipase, has been involved in the pathophysiology of cardiometabolic diseases. The impact of bariatric surgery on circulating ATX levels is unknown. We examined the short- (24 h, 5 days) and longer-term (6 and 12 months) impact of bariatric surgery; as well as the short-term effect of caloric restriction (CR) on plasma ATX levels in patients with severe obesity. We measured ATX levels in 69 men and women (mean age: 41 ± 11 years, body mass index: 49.8 ± 7.1 kg/m ), before and after biliopancreatic diversion with duodenal switch surgery (BPD-DS) as well as in a control group (patients with severe obesity without surgery; n = 34). We also measured ATX levels in seven patients with severe obesity and type 2 diabetes who underwent a 3-day CR protocol before their BPD-DS. At baseline, ATX levels were positively associated with body mass index, fat mass, insulin resistance (HOMA-IR) as well as insulin and leptin levels and negatively with fat-free mass. ATX concentrations decreased 26.2% at 24 h after BPD-DS (342.9 ± 152.3 pg/mL to 253.2 ± 68.9 pg/mL, P < 0.0001) and by 16.4% at 12 months after BPD-DS (342.9 ± 152.3 pg/mL to 286.8 ± 182.6 pg/mL, P = 0.04). ATX concentrations were unchanged during follow-up in the control group (P = 0.4), and not influenced by short-term CR. In patients with severe obesity, bariatric surgery induced a rapid and sustained decrease in plasma ATX levels. Acute changes in ATX may not be explained by bariatric surgery-induced CR.
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http://dx.doi.org/10.14814/phy2.14004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6395307PMC
March 2019

Impact of a one-year lifestyle modification program on cholesterol efflux capacities in men with abdominal obesity and dyslipidemia.

Am J Physiol Endocrinol Metab 2018 10 5;315(4):E460-E468. Epub 2018 Jun 5.

Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec, Quebec, QC, Canada.

Cholesterol efflux capacities (CECs) are negatively associated with cardiovascular disease risk, irrespective of plasma high-density lipoprotein (HDL) cholesterol levels. Whether interventions targeting lifestyle improve HDL-CECs is unknown. Our objective was to determine whether improving dietary quality and increasing physical activity levels improves HDL-CECs in men with abdominal obesity and dyslipidemia. Our study sample included men (48 ± 8.5 yr) with an elevated waist circumference (≥90 cm) associated with dyslipidemia (triglycerides ≥1.69 and/or HDL cholesterol <1.03 mmol/l); 113 men completed a 1-yr intervention, consisting of a healthy eating and physical activity/exercise program, and 32 were included in a control group. An oral lipid tolerance test (OLTT) was performed in a subsample of 28 men who completed the intervention, and blood was collected every 2 h for 8 h. HDL-CECs were measured using [H]cholesterol-labeled J774 macrophages and HepG2 hepatocytes. The lifestyle modification program led to an overall improvement in the cardiometabolic risk profile, increases in J774-HDL-CEC by 14.1% (+0.88 ± 1.09%, P < 0.0001), HepG2-HDL-CEC by 3.4% (+0.17 ± 0.75%, P = 0.01), and HDL cholesterol and apolipoprotein A-1 levels (13.5%, P < 0.0001 and 14.9%, P < 0.0001, respectively). J774-HDL-CECs and HepG2-HDL-CECs did not change in the control group. The best predictor for changes in HDL-CEC was apolipoprotein A-1 level. The lifestyle modification program also improved HDL-CEC response in postprandial lipemia during an OLTT. HDL-CEC did not change during the OLTT. Our results suggest that increasing physical activity levels and improving diet quality can have a positive impact on both HDL quantity and quality in men with abdominal obesity and dyslipidemia.
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http://dx.doi.org/10.1152/ajpendo.00127.2018DOI Listing
October 2018

Longitudinal Changes in Cholesterol Efflux Capacities in Patients With Coronary Artery Disease Undergoing Lifestyle Modification Therapy.

J Am Heart Assoc 2018 06 1;7(11). Epub 2018 Jun 1.

Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec, Canada

Background: Our objective was to identify the determinants of high-density lipoprotein cholesterol efflux capacity (HDL-CEC) changes in patients with coronary artery disease who participated in a lifestyle modification program aimed at increasing physical activity levels and improving diet quality.

Methods And Results: A total of 86 men with coronary artery disease aged between 35 and 80 years participated in a 1-year lifestyle modification program that aimed to achieve a minimum of 150 minutes of aerobic physical activity weekly and improve diet quality. HDL-CECs were measured before and after the 1-year intervention using H-cholesterol-labeled J774 and HepG2 cells. Visceral, subcutaneous, and cardiac adipose tissue levels were assessed before and after the intervention using magnetic resonance imaging. Lipoprotein particle size and concentrations were measured by proton nuclear magnetic resonance spectroscopy and a complete lipoprotein-lipid profile was obtained. At baseline, the best correlate of HDL-CECs were apolipoprotein AI (=0.35, <0.0001) and high-density lipoprotein cholesterol (=0.21, <0.0001) for J774-HDL-CECs and HepG2-HDL-CECs, respectively. Baseline and longitudinal changes in HDL-CECs were associated with several lipoprotein size and concentration indices, although high-density lipoprotein cholesterol was the best predictor of longitudinal changes in J774-HDL-CECs (=0.18, =0.002) and apolipoprotein AI was found to be the best predictor of longitudinal changes in HepG2 cholesterol efflux capacities (=0.21, =0.002).

Conclusions: Results of this study suggest that increases in high-density lipoprotein cholesterol and apolipoprotein AI levels typically observed in patients with coronary artery disease undergoing healthy lifestyle modification therapy may be indicative of higher plasma concentrations of functional high-density lipoprotein particles.
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http://dx.doi.org/10.1161/JAHA.118.008681DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6015361PMC
June 2018

Treatment with a novel agent combining docosahexaenoate and metformin increases protectin DX and IL-6 production in skeletal muscle and reduces insulin resistance in obese diabetic db/db mice.

Diabetes Obes Metab 2017 03 9;19(3):313-319. Epub 2016 Dec 9.

Axe Cardiologie Quebec Heart and Lung Research Institute, Laval University, Québec, Canada.

Aims: To compare the therapeutic potential of TP-113, a unique molecular entity linking DHA with metformin, for alleviating insulin resistance in obese diabetic mice through the PDX/IL-6 pathway.

Material And Methods: We utilized the generically obese diabetic db/db mouse model for all experiments. Initial studies investigated both a dose and time course response. These results were then utilized to design a long-term (5 week) treatment protocol. Mice were gavaged twice daily with 1 of 3 treatments: 200 mg/kg BW TP113, an equivalent dose of metformin alone (70 mg/kg BW) or water. Whole-body insulin sensitivity was measured using the hyperinsulinaemic-isoglycaemic clamp procedure in awake unrestrained mice.

Results: We first confirmed that acute TP-113 treatment raises PDX and IL-6 levels in skeletal muscle. We next tested the long-term glucoregulatory effect of oral TP-113 in obese diabetic db/db mice and compared its effect to an equivalent dose of metformin. A 5-week oral treatment with TP-113 reduced insulin resistance compared to both vehicle treatment and metformin alone, revealed by the determination of whole-body insulin sensitivity for glucose disposal using the clamp technique. This insulin-sensitizing effect was explained primarily by improvement of insulin action to suppress hepatic glucose production in TP-113-treated mice. These effects of TP-113 were greater than that of an equivalent dose of metformin, indicating that TP-113 increases metformin efficacy for reducing insulin resistance.

Conclusion: We conclude that TP-113 improves insulin sensitivity in obese diabetic mice through activation of the PDX/IL-6 signaling axis in skeletal muscle and improved glucoregulatory action in the liver.
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http://dx.doi.org/10.1111/dom.12818DOI Listing
March 2017

Low-Molecular-Weight Peptides from Salmon Protein Prevent Obesity-Linked Glucose Intolerance, Inflammation, and Dyslipidemia in LDLR-/-/ApoB100/100 Mice.

J Nutr 2015 Jul 20;145(7):1415-22. Epub 2015 May 20.

Department of Medicine, Quebec Heart and Lung Institute, Institute of Nutrition and Functional Foods, and

Background: We previously reported that fish proteins can alleviate metabolic syndrome (MetS) in obese animals and human subjects.

Objectives: We tested whether a salmon peptide fraction (SPF) could improve MetS in mice and explored potential mechanisms of action.

Methods: ApoB(100) only, LDL receptor knockout male mice (LDLR(-/-)/ApoB(100/100)) were fed a high-fat and -sucrose (HFS) diet (25 g/kg sucrose). Two groups were fed 10 g/kg casein hydrolysate (HFS), and 1 group was additionally fed 4.35 g/kg fish oil (FO; HFS+FO). Two other groups were fed 10 g SPF/kg (HFS+SPF), and 1 group was additionally fed 4.35 g FO/kg (HFS+SPF+FO). A fifth (reference) group was fed a standard feed pellet diet. We assessed the impact of dietary treatments on glucose tolerance, adipose tissue inflammation, lipid homeostasis, and hepatic insulin signaling. The effects of SPF on glucose uptake, hepatic glucose production, and inducible nitric oxide synthase activity were further studied in vitro with the use of L6 myocytes, FAO hepatocytes, and J774 macrophages.

Results: Mice fed HFS+SPF or HFS+SPF+FO diets had lower body weight (protein effect, P = 0.024), feed efficiency (protein effect, P = 0.018), and liver weight (protein effect, P = 0.003) as well as lower concentrations of adipose tissue cytokines and chemokines (protein effect, P ≤ 0.003) compared with HFS and HFS+FO groups. They also had greater glucose tolerance (protein effect, P < 0.001), lower activation of the mammalian target of rapamycin complex 1/S6 kinase 1/insulin receptor substrate 1 (mTORC1/S6K1/IRS1) pathway, and increased insulin signaling in liver compared with the HFS and HFS+FO groups. The HFS+FO, HFS+SPF, and HFS+SPF+FO groups had lower plasma triglycerides (protein effect, P = 0.003; lipid effect, P = 0.002) than did the HFS group. SPF increased glucose uptake and decreased HGP and iNOS activation in vitro.

Conclusions: SPF reduces obesity-linked MetS features in LDLR(-/-)/ApoB(100/100) mice. The anti-inflammatory and glucoregulatory properties of SPF were confirmed in L6 myocytes, FAO hepatocytes, and J774 macrophages.
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http://dx.doi.org/10.3945/jn.114.208215DOI Listing
July 2015

Transgenic ω-3 PUFA enrichment alters morphology and gene expression profile in adipose tissue of obese mice: Potential role for protectins.

Metabolism 2015 Jun 3;64(6):666-76. Epub 2015 Feb 3.

Department of Medicine, Québec Heart and Lung Institute, Université Laval, Ste-Foy, Québec, Canada and Laval University Hospital Research Center, Metabolism, Vascular and Renal Health Axis, Ste-Foy, Québec, Canada. Electronic address:

Objective: Dietary administration of ω-3 polyunsaturated fatty acids (PUFA) is often associated with altered adipose tissue (AT) morphology and/or function in obese mice. Yet, it is unclear whether this is an indirect consequence of reduced weight gain or results from direct actions of ω-3 PUFA. Here we studied the AT of high fat (HF)-fed fat-1 transgenic mice that convert endogenous ω-6 to ω-3 PUFA while maintaining equivalent fat accretion as their wild-type (WT) counterparts.

Materials And Methods: Adipocyte size profiling, Affymetrix microarray pathway analysis, qPCR and protectin identification and analysis were performed in epididymal AT from hemizygous fat-1(+/-) mice and their wild type littermates that had been fed a HF diet for 8weeks from 6weeks of age.

Results: Despite equivalent fat pad mass, we found that epididymal AT from HF-fed transgenic animals possesses fewer large and very large but more mid-size adipocytes compared to WT mice. In order to better understand the underlying mechanisms contributing to the observed alteration in adipocyte size we performed an Affymetrix microarray. Pathway analysis of these data highlighted adipogenesis, cholesterol biosynthesis, insulin signaling, prostaglandin synthesis/regulation and small ligand GPCRs as points where differentially expressed genes were significantly overrepresented. Observed changes were confirmed for four candidate genes: Cnr1, Cnr2, Faah and Pparg by qPCR. Finally we demonstrated that protectin DX is present in AT and that protectin DX and protectin D1 promote comparable PPARγ transcriptional activity.

Conclusions: These data provide unprecedented evidence that ω-3 PUFA coordinately regulate AT gene expression programs in a manner that is independent of restriction of weight gain or fat accrual and highlight an important influence of ω-3 PUFA on adipogenesis. Furthermore we provide primary evidence suggesting that protectins likely contribute to these effects via their influence on PPARγ.
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http://dx.doi.org/10.1016/j.metabol.2015.01.017DOI Listing
June 2015

Protectin DX alleviates insulin resistance by activating a myokine-liver glucoregulatory axis.

Nat Med 2014 Jun 11;20(6):664-9. Epub 2014 May 11.

1] Department of Medicine, Québec Heart and Lung Institute, Laval University, Québec, Québec, Canada. [2] Institute of Nutrition and Functional Foods, Laval University, Québec, Québec, Canada.

We previously demonstrated that low biosynthesis of ω-3 fatty acid-derived proresolution mediators, termed protectins, is associated with an impaired global resolution capacity, inflammation and insulin resistance in obese high-fat diet-fed mice. These findings prompted a more direct study of the therapeutic potential of protectins for the treatment of metabolic disorders. Herein we show that protectin DX (PDX) exerts an unanticipated glucoregulatory activity that is distinct from its anti-inflammatory actions. We found that PDX selectively stimulated the release of the prototypic myokine interleukin-6 (IL-6) from skeletal muscle and thereby initiated a myokine-liver signaling axis, which blunted hepatic glucose production via signal transducer and activator of transcription 3 (STAT3)-mediated transcriptional suppression of the gluconeogenic program. These effects of PDX were abrogated in Il6-null mice. PDX also activated AMP-activated protein kinase (AMPK); however, it did so in an IL-6-independent manner. Notably, we demonstrated that administration of PDX to obese diabetic db/db mice raises skeletal muscle IL-6 levels and substantially improves their insulin sensitivity without any impact on adipose tissue inflammation. Our findings thus support the development of PDX-based selective muscle IL-6 secretagogues as a new class of therapy for the treatment of insulin resistance and type 2 diabetes.
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http://dx.doi.org/10.1038/nm.3549DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4978533PMC
June 2014

Anti-diabetic and antihypertensive activities of two flaxseed protein hydrolysate fractions revealed following their simultaneous separation by electrodialysis with ultrafiltration membranes.

Food Chem 2014 Feb 29;145:66-76. Epub 2013 Jul 29.

Department of Food Science and Nutrition, Université Laval, Québec, Québec G1V 0A6, Canada; Institute of Nutrition and Functionnal Foods (INAF), Université Laval, Québec, Québec G1V 0A6, Canada.

Flaxseed protein hydrolysate has been fractionated by electrodialysis with two ultrafiltration membranes (20 and 50 kDa) stacked in the system for the recovery of two specific cationic peptide fractions (KCl-F1 and KCl-F2). After 360 min of treatment, peptide migration increased as a function of time in KCl compartments. Moreover, the use of two different ultrafiltration membrane allowed concentration of the 300-400 and 400-500 Da molecular weight range peptides in the KCl-F1 and KCl-F2 fractions, respectively, compared to the initial hydrolysate. After mass spectrometry analysis, higher amounts of low molecular weight peptides were recovered in the KCl-F2 compartment while relatively higher molecular weight peptides were more detected in the KCl-F1 compartment. Amino acid analysis showed that His, Lys and Arg were especially concentrated in the KCl compartments. Finally, glucose-transport assay demonstrated that the KCl-F2 fraction increased glucose uptake while oral administration of KCl-F1 and final FPH decreased systolic blood pressure.
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http://dx.doi.org/10.1016/j.foodchem.2013.07.108DOI Listing
February 2014

t-10, c-12 CLA dietary supplementation inhibits atherosclerotic lesion development despite adverse cardiovascular and hepatic metabolic marker profiles.

PLoS One 2012 20;7(12):e52634. Epub 2012 Dec 20.

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada.

Animal and human studies have indicated that fatty acids such as the conjugated linoleic acids (CLA) found in milk could potentially alter the risk of developing metabolic disorders including diabetes and cardiovascular disease (CVD). Using susceptible rodent models (apoE(-/-) and LDLr(-/-) mice) we investigated the interrelationship between mouse strain, dietary conjugated linoleic acids and metabolic markers of CVD. Despite an adverse metabolic risk profile, atherosclerosis (measured directly by lesion area), was significantly reduced with t-10, c-12 CLA and mixed isomer CLA (Mix) supplementation in both apoE(-/-) (p<0.05, n = 11) and LDLr(-/-) mice (p<0.01, n = 10). Principal component analysis was utilized to delineate the influence of multiple plasma and tissue metabolites on the development of atherosclerosis. Group clustering by dietary supplementation was evident, with the t-10, c-12 CLA supplemented animals having distinct patterns, suggestive of hepatic insulin resistance, regardless of mouse strain. The effect of CLA supplementation on hepatic lipid and fatty acid composition was explored in the LDLr(-/-) strain. Dietary supplementation with t-10, c-12 CLA significantly increased liver weight (p<0.05, n = 10), triglyceride (p<0.01, n = 10) and cholesterol ester content (p<0.01, n = 10). Furthermore, t-10, c-12 CLA also increased the ratio of 18∶1 to 18∶0 fatty acid in the liver suggesting an increase in the activity of stearoyl-CoA desaturase. Changes in plasma adiponectin and liver weight with t-10, c-12 CLA supplementation were evident within 3 weeks of initiation of the diet. These observations provide evidence that the individual CLA isomers have divergent mechanisms of action and that t-10, c-12 CLA rapidly changes plasma and liver markers of metabolic syndrome, despite evidence of reduction in atherosclerosis.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0052634PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527580PMC
June 2013

Conjugated linoleic acid supplementation for 8 weeks does not affect body composition, lipid profile, or safety biomarkers in overweight, hyperlipidemic men.

J Nutr 2011 Jul 18;141(7):1286-91. Epub 2011 May 18.

Department of Food Science and Nutrition, and Institute of Nutraceuticals and Functional Foods, Laval University, Quebec, QC G1V 0A6, Canada.

The usefulness of conjugated linoleic acid (CLA) as a nutraceutical remains ambiguous. Our objective was, therefore, to investigate the effect of CLA on body composition, blood lipids, and safety biomarkers in overweight, hyperlipidemic men. A double-blinded, 3-phase crossover trial was conducted in overweight (BMI ≥ 25 kg/m(2)), borderline hypercholesterolemic [LDL-cholesterol (C) ≥ 2.5 mmol/L] men aged 18-60 y. During three 8-wk phases, each separated by a 4-wk washout period, 27 participants consumed under supervision in random order 3.5 g/d of safflower oil (control), a 50:50 mixture of trans 10, cis 12 and cis 9, trans 11 (c9, t11) CLA:Clarinol G-80, and c9, t11 isomer:c9, t11 CLA. At baseline and endpoint of each phase, body weight, body fat mass, and lean body mass were measured by DXA. Blood lipid profiles and safety biomarkers, including insulin sensitivity, blood concentrations of adiponectin, and inflammatory (high sensitive-C-reactive protein, TNFα, and IL-6) and oxidative (oxidized-LDL) molecules, were measured. The effect of CLA consumption on fatty acid oxidation was also assessed. Compared with the control treatment, the CLA treatments did not affect changes in body weight, body composition, or blood lipids. In addition, CLA did not affect the β-oxidation rate of fatty acids or induce significant alterations in the safety markers tested. In conclusion, although no detrimental effects were caused by supplementation, these results do not confirm a role for CLA in either body weight or blood lipid regulation in humans.
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http://dx.doi.org/10.3945/jn.110.135087DOI Listing
July 2011

Conjugated linoleic acid and atherosclerosis: studies in animal models.

Biochem Cell Biol 2008 Aug;86(4):293-301

Department of Biochemistry & Molecular Biology, Dalhousie University, Halifax, NS, Canada.

Conjugated linoleic acids (CLA) are isomeric forms of linoleic acid (LA) containing two conjugated sites of unsaturation. The most abundant dietary form of CLA is the cis-9,trans-11 (c-9,t-11) isomer that is found in the fatty tissues and milk of ruminant animals. CLA can also be acquired by ingestion of supplements, which are usually equimolar mixtures of the c-9,t-11 and t-10,c-12 CLA. For more than a decade, the potential for CLA to modify atherosclerosis in animal models has been examined. However, to date, the studies have failed to reach consensus on whether CLA can be effective in reducing the incidence or severity of atherosclerotic lesions, or whether or not plasma lipid and lipoprotein levels can be improved with CLA supplementation. This review will examine the evidence for and against a role for CLA in atherosclerosis, with a focus on the rabbit, the hamster, and the apoE-deficient mouse.
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http://dx.doi.org/10.1139/o08-070DOI Listing
August 2008

Conjugated linoleic acid isomers have no effect on atherosclerosis and adverse effects on lipoprotein and liver lipid metabolism in apoE-/- mice fed a high-cholesterol diet.

Atherosclerosis 2008 Oct 15;200(2):294-302. Epub 2008 Feb 15.

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada.

Dietary supplementation with conjugated linoleic acid (CLA) has been shown, in several animal models, to decrease the development of atherosclerosis. The mechanism behind the anti-atherogenic properties of CLA is not clear. The objectives of this study were to determine the effect of CLA on atherosclerosis, lipoprotein and liver lipid metabolism, and plasma adiponectin and insulin in apoE(-/-) mice fed an atherogenic (16%, w/w fat; 1.25%, w/w cholesterol) diet. Mice were fed the diet with or without supplementation of linoleic acid (LA), c-9,t-11 CLA, t-10,c-12 CLA, or a 1:1 mixture of the two CLA isomers, at a concentration of 0.5% (w/w), for 12 weeks. Relative to the LA group, CLA supplementation had no significant effect on the lesion area in either en face preparations of the aorta or in aortic root cross-sections. Plasma triacylglycerol and cholesterol concentrations were higher in the t-10,c-12 CLA group than all other treatment groups and liver weight was also increased in this group due to a three-fold increase in liver triacylglycerol. Supplementation with t-10,c-12 CLA or mixed CLA reduced plasma adiponectin levels, whereas t-10,c-12 CLA increased plasma insulin levels. Liver triglycerides correlated directly with blood glucose and plasma insulin and inversely with plasma adiponectin. We conclude that dietary supplementation with CLA does not affect atherosclerosis of the apoE(-/-) mouse on a high-cholesterol diet. Furthermore, t-10,c-12 CLA causes adverse changes in adipocyte function and plasma and liver lipid metabolism, which are partially ameliorated by the inclusion of the c-9,t-11 CLA isomer.
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http://dx.doi.org/10.1016/j.atherosclerosis.2007.12.040DOI Listing
October 2008

Effect of conjugated linoleic acid isomers on lipoproteins and atherosclerosis in the Syrian Golden hamster.

Biochim Biophys Acta 2005 Jun;1734(3):269-76

Department of Biochemistry and Molecular Biology, Dalhousie University, 5850 College Street, Halifax, Nova Scotia, Canada B3H 1X5.

Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of linoleic acid (LA, C18:2 cis-9, cis-12) that are reported to have important biological activities, including protection against atherosclerosis. In this study, the potential role of the individual cis-9, trans-11 and trans-10, cis-12 isomers of CLA in atherogenesis were compared with LA in the Syrian Golden hamster. Supplementation of a high-fat, high-cholesterol diet (HFHC) with 1% (w/w) cis-9, trans-11 CLA or trans-10, cis-12 CLA did not significantly affect plasma cholesterol levels compared to supplementation with 1% (w/w) LA. Very low density lipoprotein cholesterol (VLDL-C) was lower and plasma triglycerides (TG) were higher in diets where C18:2 fatty acid was added to the HFHC diet, but neither the cis-9, trans-11 CLA group nor trans-10, cis-12 CLA group was significantly different from the LA control group. CLA supplementation did not significantly affect low density lipoprotein cholesterol (LDL-C). Trans-10, cis-12 CLA increased high density lipoprotein cholesterol (HDL-C) levels compared to LA or cis-9, trans-11 CLA (P<0.02), and although the ratio of non-HDL-C:HDL-C in the cis-9, trans-11 CLA group (1.11+/-0.54) and the trans-10, cis-12 CLA group (1.11+/-0.21) was lower than the LA group (1.29+/-0.45), the reduction did not reach statistical significance. Atherosclerosis was assessed in the ascending aorta by measuring the number of aortic cross-sections containing Oil Red O-stained intimal lesions. Compared to the LA group (60+/-11%), both the cis-9, trans-11 CLA group (38+/-8%) and the trans-10, cis-12 CLA group (28+/-7%) had fewer sections displaying a fatty streak lesion, although the differences did not reach statistical significance. These results suggest that individual CLA isomers may reduce atherosclerotic lesion development in the hamster, but when compared to LA, the apparent atheroprotective effects do not correlate with beneficial changes in lipoprotein profile.
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http://dx.doi.org/10.1016/j.bbalip.2005.04.007DOI Listing
June 2005

Conjugated linoleic acids, atherosclerosis, and hepatic very-low-density lipoprotein metabolism.

Am J Clin Nutr 2004 06;79(6 Suppl):1169S-1174S

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Canada.

Conjugated linoleic acids (CLAs) are isomeric forms of the 18:2 fatty acid that contain conjugated sites of unsaturation. Although CLAs are minor components of the diet, they have many reported biological activities. For nearly a decade, the potential for CLA to modify the atherosclerotic process has been examined in animal models, and studies of supplementation of the human diet with CLA were started with the anticipation that such an intervention could also reduce the risk of cardiovascular disease. Central to the hypothesis is the expectation that dietary modification could alter plasma lipid and lipoprotein metabolism toward a more cardioprotective profile. This review examines the evidence in support of the hypothesis and the mechanistic studies that lend support for a role of CLA in hepatic lipid and lipoprotein metabolism. Although there are still limited studies in strong support of a role for CLA in the reduction of early atherosclerotic lesions, there has been considerable progress in defining the mechanisms of CLA action. CLA could primarily modulate the metabolism of fatty acids in the liver. The tools are now available to examine isomer-specific effects of CLA on hepatic lipid and lipoprotein metabolism and the potential of CLA to modify hepatic gene expression patterns. Additional animal and cell culture studies will increase our understanding of these unusual fatty acids and their potential for health benefits in humans.
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http://dx.doi.org/10.1093/ajcn/79.6.1169SDOI Listing
June 2004

Using the Essential Public Health Services as strategic leverage to strengthen the public health response to diabetes.

Public Health Rep 2004 May-Jun;119(3):311-21

Program Development Branch, Division of Diabetes Translation, Centers for Disease Control and Prevention, Atlanta, GA 30341-4002, USA.

If current trends continue, health systems will soon be overwhelmed by type 2 diabetes mellitus. Successful population-based diabetes prevention and control efforts require a sound and continually improving infrastructure. In states and U.S. territories, the Diabetes Prevention and Control Programs supported by the U.S. Centers for Disease Control and Prevention's Division of Diabetes Translation serve as a fulcrum for building and refining the infrastructure that links diverse and dynamic partners dedicated to increasing the years and quality of life and achieving health equity among people with and at risk for diabetes. The National Public Health Performance Standards offer a conceptual framework that articulates the requisite infrastructure and services provided by an interconnected network of intersectoral partners to strengthen the public health response to diabetes. These standards associated with the Essential Public Health Services are valuable tools to assess the status of the performance of the health system's infrastructure to guide improvement. The process of engaging system partners in a system-wide assessment informs and leverages cross-sectoral assets to improve health outcomes for citizens in communities shouldering the growing burden of diabetes.
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http://dx.doi.org/10.1016/j.phr.2004.04.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1497627PMC
July 2004

Use of data from the Behavioral Risk Factor Surveillance System optional diabetes module by states.

J Public Health Manag Pract 2003 Nov;Suppl:S52-5

Program Development Branch, Division of Diabetes Translation, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, 4770 Buford Highway, NE, Mailstop K-10, Atlanta, GA 30341, USA.

An optional diabetes module of the Behavioral Risk Factor Surveillance System was first made available to states in 1993. In 2002, 49 states administered this module. In October 2001 we asked state Diabetes Prevention and Control Program coordinators to complete a two-part questionnaire regarding the use of data from the diabetes module and their usefulness in guiding programmatic activities. Seventy percent of state coordinators reported using data from at least one module question to perform program evaluation, develop publications, and development of community interventions; 45 percent of coordinators used data from at least one module question for activities related to passage of legislation. Questions on self monitoring of blood glucose, hemoglobin A1c test, annual foot exam, annual dilated eye exam, and diabetes education were rated as highly useful by the state coordinators. The results from the optional diabetes module are widely used by states and are essential to Diabetes Prevention and Control Program activities. It is important that the optional diabetes module continue to be included in each state's yearly Behavioral Risk Factor Surveillance System.
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http://dx.doi.org/10.1097/00124784-200311001-00009DOI Listing
November 2003

Treatment of plantar verrucae using 2% sodium salicylate iontophoresis.

Phys Ther 2002 Dec;82(12):1184-91

Marshfield Clinic-Wausau Center, 2727 Plaza Dr, Wausau, WI 54401-4192, USA.

Background And Purpose: Iontophoretic sodium salicylate treatment of plantar warts was studied.

Subjects: Twenty patients with 104 plantar verrucae were studied.

Methods: Two percent sodium salicylate solution was administered iontophoretically (22.5 mA-minute/electrode, 3 treatments at 6- to 9-day intervals). Results. Nineteen subjects were followed. Verrucae area declined in 15 subjects (78.9%) and increased in 2 subjects (10.5%). One subject (5.3%) no longer had verrucae, and 1 subject (5.3%) exhibited no change. Overall, the number of verrucae and total area decreased. Four of 6 subjects (66.6%) with initial complaints of load-bearing pain reported diminished pain following treatment. Two subjects whose verrucae's size increased reported an increase in pain at the end of the study.

Discussion And Conclusion: Sodium salicylate iontophoresis appeared to compare favorably with other office-based interventions in diminishing the size of plantar warts and their associated pain. Application of iontophoresis to weight-bearing surfaces in some subjects appeared to decrease the pain and scarring associated with freezing and electrocautery and the fixation problems associated with medicated patches.
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December 2002