Publications by authors named "Markku Taittonen"

17 Publications

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Adenosine/A2B Receptor Signaling Ameliorates the Effects of Aging and Counteracts Obesity.

Cell Metab 2020 Jul 25;32(1):56-70.e7. Epub 2020 Jun 25.

Institute of Pharmacology and Toxicology, University Hospital, University of Bonn, 53127 Bonn, Germany. Electronic address:

The combination of aging populations with the obesity pandemic results in an alarming rise in non-communicable diseases. Here, we show that the enigmatic adenosine A2B receptor (A2B) is abundantly expressed in skeletal muscle (SKM) as well as brown adipose tissue (BAT) and might be targeted to counteract age-related muscle atrophy (sarcopenia) as well as obesity. Mice with SKM-specific deletion of A2B exhibited sarcopenia, diminished muscle strength, and reduced energy expenditure (EE), whereas pharmacological A2B activation counteracted these processes. Adipose tissue-specific ablation of A2B exacerbated age-related processes and reduced BAT EE, whereas A2B stimulation ameliorated obesity. In humans, A2B expression correlated with EE in SKM, BAT activity, and abundance of thermogenic adipocytes in white fat. Moreover, A2B agonist treatment increased EE from human adipocytes, myocytes, and muscle explants. Mechanistically, A2B forms heterodimers required for adenosine signaling. Overall, adenosine/A2B signaling links muscle and BAT and has both anti-aging and anti-obesity potential.
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http://dx.doi.org/10.1016/j.cmet.2020.06.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7437516PMC
July 2020

BATLAS: Deconvoluting Brown Adipose Tissue.

Cell Rep 2018 10;25(3):784-797.e4

Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland. Electronic address:

Recruitment and activation of thermogenic adipocytes have received increasing attention as a strategy to improve systemic metabolic control. The analysis of brown and brite adipocytes is complicated by the complexity of adipose tissue biopsies. Here, we provide an in-depth analysis of pure brown, brite, and white adipocyte transcriptomes. By combining mouse and human transcriptome data, we identify a gene signature that can classify brown and white adipocytes in mice and men. Using a machine-learning-based cell deconvolution approach, we develop an algorithm proficient in calculating the brown adipocyte content in complex human and mouse biopsies. Applying this algorithm, we can show in a human weight loss study that brown adipose tissue (BAT) content is associated with energy expenditure and the propensity to lose weight. This online available tool can be used for in-depth characterization of complex adipose tissue samples and may support the development of therapeutic strategies to increase energy expenditure in humans.
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http://dx.doi.org/10.1016/j.celrep.2018.09.044DOI Listing
October 2018

Cannabinoid Type 1 Receptors Are Upregulated During Acute Activation of Brown Adipose Tissue.

Diabetes 2018 07 12;67(7):1226-1236. Epub 2018 Apr 12.

Turku PET Centre, University of Turku, Turku, Finland

Activating brown adipose tissue (BAT) could provide a potential approach for the treatment of obesity and metabolic disease in humans. Obesity is associated with upregulation of the endocannabinoid system, and blocking the cannabinoid type 1 receptor (CB1R) has been shown to cause weight loss and to decrease cardiometabolic risk factors. These effects may be mediated partly via increased BAT metabolism, since there is evidence that CB1R antagonism activates BAT in rodents. To investigate the significance of CB1R in BAT function, we quantified the density of CB1R in human and rodent BAT using the positron emission tomography radioligand [F]FMPEP- and measured BAT activation in parallel with the glucose analog [F]fluorodeoxyglucose. Activation by cold exposure markedly increased CB1R density and glucose uptake in the BAT of lean men. Similarly, β3-receptor agonism increased CB1R density in the BAT of rats. In contrast, overweight men with reduced BAT activity exhibited decreased CB1R in BAT, reflecting impaired endocannabinoid regulation. Image-guided biopsies confirmed CB1R mRNA expression in human BAT. Furthermore, CB1R blockade increased glucose uptake and lipolysis of brown adipocytes. Our results highlight that CB1Rs are significant for human BAT activity, and the CB1Rs provide a novel therapeutic target for BAT activation in humans.
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http://dx.doi.org/10.2337/db17-1366DOI Listing
July 2018

miR-125b affects mitochondrial biogenesis and impairs brite adipocyte formation and function.

Mol Metab 2016 Aug 15;5(8):615-625. Epub 2016 Jun 15.

Univ. Nice Sophia Antipolis, CNRS, Inserm, iBV, 06100 Nice, France. Electronic address:

Objective: In rodents and humans, besides brown adipose tissue (BAT), islands of thermogenic adipocytes, termed "brite" (brown-in-white) or beige adipocytes, emerge within white adipose tissue (WAT) after cold exposure or β3-adrenoceptor stimulation, which may protect from obesity and associated diseases. microRNAs are novel modulators of adipose tissue development and function. The purpose of this work was to characterize the role of microRNAs in the control of brite adipocyte formation.

Methods/results: Using human multipotent adipose derived stem cells, we identified miR-125b-5p as downregulated upon brite adipocyte formation. In humans and rodents, miR-125b-5p expression was lower in BAT than in WAT. In vitro, overexpression and knockdown of miR-125b-5p decreased and increased mitochondrial biogenesis, respectively. In vivo, miR-125b-5p levels were downregulated in subcutaneous WAT and interscapular BAT upon β3-adrenergic receptor stimulation. Injections of an miR-125b-5p mimic and LNA inhibitor directly into WAT inhibited and increased β3-adrenoceptor-mediated induction of UCP1, respectively, and mitochondrial brite adipocyte marker expression and mitochondriogenesis.

Conclusion: Collectively, our results demonstrate that miR-125b-5p plays an important role in the repression of brite adipocyte function by modulating oxygen consumption and mitochondrial gene expression.
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http://dx.doi.org/10.1016/j.molmet.2016.06.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5021678PMC
August 2016

Visfatin expression analysis in association with recruitment and activation of human and rodent brown and brite adipocytes.

Adipocyte 2016 Apr-Jun;5(2):186-95. Epub 2015 Dec 9.

Univ. Nice-Sophia Antipolis, UFR Medecine, Nice, France; CNRS, iBV, UMR, 7277, Nice, France; INSERM, iBV, U1091, Nice, France.

Human brown adipocytes are able to burn fat and glucose and are now considered as a potential strategy to treat obesity, type 2 diabetes and metabolic disorders. Besides their thermogenic function, brown adipocytes are able to secrete adipokines. One of these is visfatin, a nicotinamide phosphoribosyltransferase involved in nicotinamide dinucleotide synthesis, which is known to participate in the synthesis of insulin by pancreatic β cells. In a therapeutic context, it is of interest to establish whether a potential correlation exists between brown adipocyte activation and/or brite adipocyte recruitment, and adipokine expression. We analyzed visfatin expression, as a pre-requisite to its secretion, in rodent and human biopsies and cell models of brown/brite adipocytes. We found that visfatin was preferentially expressed in mature adipocytes and that this expression was higher in brown adipose tissue of rodents compared to other fat depots. However, using various rodent models we were unable to find any correlation between visfatin expression and brown or brite adipocyte activation or recruitment. Interestingly, the situation is different in humans where visfatin expression was found to be equivalent between white and brown or brite adipocytes in vivo and in vitro. In conclusion, visfatin can be considered only as a rodent brown adipocyte biomarker, independently of tissue activation.
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http://dx.doi.org/10.1080/21623945.2015.1122854DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916889PMC
July 2016

Let-7i-5p represses brite adipocyte function in mice and humans.

Sci Rep 2016 06 27;6:28613. Epub 2016 Jun 27.

Univ. Nice Sophia Antipolis, iBV, UMR 7277, Nice, 06100, France.

In response to cold or β3-adrenoreceptor stimulation brown adipose tissue (BAT) promotes non-shivering thermogenesis, leading to energy dissipation. BAT has long been thought to be absent or scarce in adult humans. The recent discovery of thermogenic brite/beige adipocytes has opened the way to development of novel innovative strategies to combat overweight/obesity and associated diseases. Thus it is of great interest to identify regulatory factors that govern the brite adipogenic program. Here, we carried out global microRNA (miRNA) expression profiling on human adipocytes to identify miRNAs that are regulated upon the conversion from white to brite adipocytes. Among the miRNAs that were differentially expressed, we found that Let-7i-5p was down regulated in brite adipocytes. A detailed analysis of the Let-7i-5p levels showed an inverse expression of UCP1 in murine and human brite adipocytes both in vivo and in vitro. Functional studies with Let-7i-5p mimic in human brite adipocytes in vitro revealed a decrease in the expression of UCP1 and in the oxygen consumption rate. Moreover, the Let-7i-5p mimic when injected into murine sub-cutaneous white adipose tissue inhibited partially β3-adrenergic activation of the browning process. These results suggest that the miRNAs Let-7i-5p participates in the recruitment and the function of brite adipocytes.
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http://dx.doi.org/10.1038/srep28613DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4921928PMC
June 2016

Myocardial glucose uptake in patients with the m.3243A > G mutation in mitochondrial DNA.

J Inherit Metab Dis 2016 Jan 26;39(1):67-74. Epub 2015 Jun 26.

Research Group of Clinical Neuroscience, Neurology, University of Oulu, P.O Box 5000, FIN-90014, Oulu, Finland.

Mitochondrial mutations impair glucose oxidation and increase glucose uptake in cell cultures and lead to cardiomyopathy in patients. Here we characterize cardiac glucose uptake in 14 patients with the m.3243A > G mutation in mitochondrial DNA. The 14 patients with m.3243A > G and 13 controls were similar in age, physical activity and body mass index. Ten patients had diabetes. Left ventricular glucose uptake per tissue mass (LVGU) was measured with 2-[(18) F]fluoro-2-deoxyglucose positron emission tomography during euglycemic hyperinsulinemia. Cardiac morphology and function were assessed with magnetic resonance imaging. We found that the LVGU was 25% lower in the patients than that in the controls (P = 0.029). LVGU was inversely correlated with mutation heteroplasmy, glycated haemoglobin and fasting lactate in patients. The seven patients with mutation heteroplasmy ≥ 49% had 44% lower LVGU than the seven patients with heteroplasmy < 49%. This difference remained significant after adjustment for concurrent free fatty acid concentration or glycated haemoglobin or glucose uptake in skeletal muscle or all (p < 0.048 [All]). Patients with m.3243A > G had a lower stroke volume and a higher heart rate than the controls, whereas cardiac output and work were similar. Myocardial glucose uptake is not increased but decreased with a threshold effect pattern in patients with the m.3243A > G mutation. The glucose hypometabolism adds to the impaired cardiac energetics and likely contributes to the progression of the mitochondrial cardiomyopathy.
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http://dx.doi.org/10.1007/s10545-015-9865-1DOI Listing
January 2016

Effect of spinal cord stimulation on myocardial perfusion reserve in patients with refractory angina pectoris.

Eur Heart J Cardiovasc Imaging 2015 Apr 2;16(4):449-55. Epub 2014 Dec 2.

Turku PET Centre, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, Turku FI-20520, Finland.

Aims: Epidural spinal cord stimulation (SCS) provides symptom relief in refractory angina pectoris, but its mechanism of action remains incompletely understood. We studied effects of short-term SCS therapy on myocardial ischaemia tolerance, myocardial perfusion reserve (MPR), and endothelium-mediated vasodilatation induced by cold pressor test (CPT) in patients with refractory angina pectoris.

Methods And Results: We prospectively recruited 18 patients with refractory angina pectoris and studied them after implantation of SCS device at baseline before starting the therapy and after 3 weeks of continuous SCS therapy. Myocardial ischaemia was evaluated by dobutamine stress echocardiography. Global and regional myocardial blood flow (MBF) were measured using positron emission tomography and (15)O-water at rest, during adenosine stress, and in response to CPT. Systemic haemodynamics were comparable before and after 3 weeks of SCS at rest, during adenosine stress and during CPT. Appearance of angina pectoris induced by dobutamine stress was delayed after SCS therapy. Global MPR increased (P = 0.02) from 1.7 ± 0.6 at baseline to 2.0 ± 0.6 after 3-week SCS therapy. This was associated with a significant reduction in global MBF at rest and increase in MBF induced by adenosine in the ischaemic regions. Global MBF response to CPT was improved after SCS (0.27 ± 0.20 vs. 0.40 ± 0.15, P = 0.03).

Conclusion: Short-term SCS therapy improved myocardial ischaemia tolerance, absolute MPR, and endothelium-mediated vasomotor function in refractory angina pectoris, indicating that this therapy can alleviate myocardial perfusion abnormalities in advanced CAD.
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http://dx.doi.org/10.1093/ehjci/jeu276DOI Listing
April 2015

Trimetazidine reduces endogenous free fatty acid oxidation and improves myocardial efficiency in obese humans.

Cardiovasc Ther 2012 Dec 31;30(6):333-41. Epub 2011 Jul 31.

Turku PET Centre, University of Turku, Turku, Finland.

Introduction: The metabolic modulator trimetazidine (TMZ) has been suggested to induce a metabolic shift from myocardial fatty acid oxidation (FAO) to glucose utilization, but this mechanism remains unproven in humans. The oxidation of plasma derived FA is commonly measured in humans, whereas the contribution of FA from triglycerides stored in the myocardium has been poorly characterized.

Aims: To verify the hypothesis that TMZ induces a metabolic shift, we combined positron emission tomography (PET) and magnetic resonance spectroscopy ((1)H-MRS) to measure myocardial FAO from plasma and intracellular lipids, and myocardial glucose metabolism. Nine obese subjects were studied before and after 1 month of TMZ treatment. Myocardial glucose and FA metabolism were assessed by PET with (18)F-fluorodeoxyglucose and (11)C-palmitate. (1)H-MRS was used to measure myocardial lipids, the latter being integrated into the PET data analysis to quantify myocardial triglyceride turnover.

Results: Myocardial FAO derived from intracellular lipids was at least equal to that of plasma FAs (P = NS). BMI and cardiac work were positively associated with the oxidation of plasma derived FA (P ≤ 0.01). TMZ halved total and triglyceride-derived myocardial FAO (32.7 ± 8.0 to 19.6 ± 4.0 μmol/min and 23.7 ± 7.5 to 10.3 ± 2.7 μmol/min, respectively; P ≤ 0.05). These changes were accompanied by increased cardiac efficiency since unchanged LV work (1.6 ± 0.2 to 1.6 ± 0.1 Watt/g × 10(2), NS) was associated with decreased work energy from the intramyocardial triglyceride oxidation (1.6 ± 0.5 to 0.4 ± 0.1 Watt/g × 10(2), P = 0.036).

Conclusions: In obese subjects, we demonstrate that myocardial intracellular triglyceride oxidation significantly provides FA-derived energy for mechanical work. TMZ reduced the oxidation of triglyceride-derived myocardial FAs improving myocardial efficiency.
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http://dx.doi.org/10.1111/j.1755-5922.2011.00275.xDOI Listing
December 2012

Different metabolic responses of human brown adipose tissue to activation by cold and insulin.

Cell Metab 2011 Aug;14(2):272-9

Turku PET Centre, University of Turku, Turku, Finland.

We investigated the metabolism of human brown adipose tissue (BAT) in healthy subjects by determining its cold-induced and insulin-stimulated glucose uptake and blood flow (perfusion) using positron emission tomography (PET) combined with computed tomography (CT). Second, we assessed gene expression in human BAT and white adipose tissue (WAT). Glucose uptake was induced 12-fold in BAT by cold, accompanied by doubling of perfusion. We found a positive association between whole-body energy expenditure and BAT perfusion. Insulin enhanced glucose uptake 5-fold in BAT independently of its perfusion, while the effect on WAT was weaker. The gene expression level of insulin-sensitive glucose transporter GLUT4 was also higher in BAT as compared to WAT. In conclusion, BAT appears to be differently activated by insulin and cold; in response to insulin, BAT displays high glucose uptake without increased perfusion, but when activated by cold, it dissipates energy in a perfusion-dependent manner.
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http://dx.doi.org/10.1016/j.cmet.2011.06.012DOI Listing
August 2011

Human obesity is characterized by defective fat storage and enhanced muscle fatty acid oxidation, and trimetazidine gradually counteracts these abnormalities.

Am J Physiol Endocrinol Metab 2011 Jul 19;301(1):E105-12. Epub 2011 Apr 19.

Turku PET Centre, University of Turku, Turku, Finland.

An impaired ability to store fatty acids (FA) in subcutaneous adipose tissue (SAT) may be implicated in the pathogenesis of obesity-related diseases via overexposure of lean tissues and production of free radicals from FA oxidation (FAO). We studied regional FA metabolism in skeletal muscle and adipose tissue in humans and investigated the long-term effects of the FAO inhibitor trimetazidine on glucose and FA metabolism. Positron emission tomography (PET) and [(11)C]palmitate were used to compare FA metabolism in SAT and skeletal muscle between eight obese and eight nonobese subjects (BMI ≥/< 30 kg/m(2)). A subgroup of nine subjects underwent a 1-mo trimetazidine administration. PET with [(11)C]palmitate and [(18)F]fluorodeoxyglucose, indirect calorimetry, and MRI before and after this period were performed to characterize glucose and FA metabolism, fat masses, skeletal muscle triglyceride, and creatine contents. Obesity was characterized by a 100% elevation in FAO and a defect in the FA esterification rate constant (P < 0.05) in skeletal muscle. FA esterification was reduced by ~70% in SAT (P < 0.001) in obese vs. control subjects. The degrees of obesity and insulin resistance were both negatively associated with esterification-related parameters and positively with FAO (P < 0.05). Trimetazidine increased skeletal muscle FA esterification (P < 0.01) and mildly upregulated glucose phosphorylation (P = 0.066). Our data suggest that human obesity is characterized by a defect in tissue FA storage capability, which is accompanied by a (potentially compensatory) elevation in skeletal muscle FAO; trimetazidine diverted FA from oxidative to nonoxidative pathways and provoked an initial activation of glucose metabolism in skeletal muscle.
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http://dx.doi.org/10.1152/ajpendo.00680.2010DOI Listing
July 2011

Blood pressure and free flap oxygenation in head and neck cancer patients.

Acta Otolaryngol 2011 Jul 17;131(7):757-63. Epub 2011 Mar 17.

Department of Otorhinolaryngology - Head and Neck Surgery, Turku University Hospital, Finland.

Conclusion: This study suggests that although oxygen partial pressure in tissue (p(ti)O(2)) measurement is a feasible method for continuous postoperative monitoring of free flaps, low correlation between blood pressure (BP) and p(ti)O(2) might predict compromised overall outcome. Thus, it is of utmost importance to keep the BP optimal for adequate perfusion of re-anastomosed tissue transfers.

Objective: Optimal BP is an important factor in assuring adequate blood flow in a free flap. Tissue oxygenation in free flaps as a postoperative monitoring target is in routine clinical use in some clinics. Correlation between p(ti)O(2) and systemic BP was investigated.

Methods: Ten consecutive patients underwent resection of head and neck squamous cell carcinoma followed by microvascular reconstruction with a free microvascular flap. P(ti)O(2) of each flap was continuously monitored for 3 postoperative days with a polarographic measurement system. BP was measured invasively and continuously during the operation and during the first postoperative day at the intensive care unit. The correlation coefficient between p(ti)O(2) and BP was analysed.

Results: The correlation coefficient between p(ti)O(2) and BP was relatively high in all patients with uneventful flap survival (r (mean) = 0.63, n = 5). In flaps with haemodynamic problems or compromised flap vitality the correlation appeared low (r(mean) = -0.02, n = 5).
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http://dx.doi.org/10.3109/00016489.2011.554438DOI Listing
July 2011

Effect of caloric restriction on myocardial fatty acid uptake, left ventricular mass, and cardiac work in obese adults.

Am J Cardiol 2009 Jun 16;103(12):1721-6. Epub 2009 Apr 16.

Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland.

Obesity is associated with increased fatty acid uptake in the myocardium, and this may have deleterious effects on cardiac function. The aim of this study was to evaluate how weight loss influences myocardial metabolism and cardiac work in obese adults. Thirty-four obese (mean body mass index 33.7 +/- 0.7 kg/m(2)) but otherwise healthy subjects consumed a very low calorie diet for 6 weeks. Cardiac substrate metabolism and work were measured before and after the diet. Myocardial fatty acid uptake was measured in 18 subjects using fluorine-18-fluoro-6-thia-heptadecanoic acid and positron emission tomography, and myocardial glucose uptake was measured in 16 subjects using fluorine-18-2-fluoro-2-deoxyglucose. Myocardial structure and cardiac function were measured using magnetic resonance imaging. Consumption of the very low calorie diet decreased weight (-11.2 +/- 0.6 kg, p <0.0001). Myocardial fatty acid uptake decreased from 4.2 +/- 0.4 to 2.9 +/- 0.2 micromol/100 g/min (p <0.0001). Myocardial mass decreased by 7% (p <0.005), and cardiac work decreased by 26% (p <0.0001). Whole-body insulin sensitivity increased by 33% (p <0.01), but insulin-stimulated myocardial glucose uptake remained unchanged (p = 0.90). Myocardial triglyceride content decreased by 31% (n = 8, p = 0.076). In conclusion, weight reduction decreases myocardial fatty acid uptake in parallel with myocardial mass and cardiac work. These results show that the increased fatty acid uptake found in the hearts of obese patients can be reversed by weight loss.
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http://dx.doi.org/10.1016/j.amjcard.2009.02.025DOI Listing
June 2009

Functional brown adipose tissue in healthy adults.

N Engl J Med 2009 Apr;360(15):1518-25

Turku PET Center, University of Turku, Finland.

Using positron-emission tomography (PET), we found that cold-induced glucose uptake was increased by a factor of 15 in paracervical and supraclavicular adipose tissue in five healthy subjects. We obtained biopsy specimens of this tissue from the first three consecutive subjects and documented messenger RNA (mRNA) and protein levels of the brown-adipocyte marker, uncoupling protein 1 (UCP1). Together with morphologic assessment, which showed numerous multilocular, intracellular lipid droplets, and with the results of biochemical analysis, these findings document the presence of substantial amounts of metabolically active brown adipose tissue in healthy adult humans.
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http://dx.doi.org/10.1056/NEJMoa0808949DOI Listing
April 2009

m.3243A>G mutation in mitochondrial DNA leads to decreased insulin sensitivity in skeletal muscle and to progressive beta-cell dysfunction.

Diabetes 2009 Mar 10;58(3):543-9. Epub 2008 Dec 10.

Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland.

Objective: To study insulin sensitivity and perfusion in skeletal muscle together with the beta-cell function in subjects with the m.3243A>G mutation in mitochondrial DNA, the most common cause of mitochondrial diabetes.

Research Design And Methods: We measured skeletal muscle glucose uptake and perfusion using positron emission tomography and 2-[18F]fluoro-2-deoxyglucose and [15O]H2O during euglycemic hyperinsulinemia in 15 patients with m.3243A>G. These patients included five subjects with no diabetes as defined by the oral glucose tolerance test (OGTT) (group 1), three with GHb <6.1% and newly found diabetes by OGTT (group 2), and seven with a previously diagnosed diabetes (group 3). Control subjects consisted of 13 healthy individuals who were similar to the carriers of m.3243A>G with respect to age and physical activity. Beta-cell function was assessed using the OGTT and subsequent mathematical modeling.

Results: Skeletal muscle glucose uptake was significantly lower in groups 1, 2, and 3 than in the control subjects. The glucose sensitivity of beta-cells in group 1 patients was similar to that of the control subjects, whereas in group 2 and 3 patients, the glucose sensitivity was significantly lower. The insulin secretion parameters correlated strongly with the proportion of m.3243A>G mutation in muscle.

Conclusions: Our findings show that subjects with m.3243A>G are insulin resistant in skeletal muscle even when beta-cell function is not markedly impaired or glucose control compromised. We suggest that both the skeletal muscle insulin sensitivity and the beta-cell function are affected before the onset of the mitochondrial diabetes caused by the m.3243A>G mutation.
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http://dx.doi.org/10.2337/db08-0981DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646052PMC
March 2009

Functional evaluation of microvascular free flaps with positron emission tomography.

J Plast Reconstr Aesthet Surg 2006 ;59(2):158-65

Department of Otorhinolaryngology, Head and Neck Surgery, Turku University Central Hospital, FIN-20521 Turku, Finland.

Background: The aim of this study was to assess blood flow (BF) of microvascular free flaps studied with positron emission tomography (PET) in patients with head and neck squamous cell cancer (HNSCC) undergoing major radical surgery 3-4 weeks after high-dose radiotherapy.

Methods: Five patients underwent resection of the HNSCC of the oral cavity followed by microvascular reconstruction with a radial forearm flap. Regional BF in oral and neck tissues was measured with PET using radiolabelled water ([15O]H2O) twice (1-2 and 12-14 days, respectively) following radical surgery.

Results: In the first postoperative PET study, the median BF in the cutaneous flap area was 5.1 mL/100 g/min, and in the muscle contra-lateral to the recipient site 19.9 mL/100 g/min. A low flap-to-muscle BF ratio appeared to correlate with circulatory incongruity, and thus with poorer flap success. The follow-up study on the second postoperative week supported the results of the primary PET scan.

Conclusions: This pilot study suggests that PET using [15O]H2O is a feasible method to quantitatively evaluate BF of the whole free flap in patients operated on for oral
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http://dx.doi.org/10.1016/j.bjps.2005.04.016DOI Listing
June 2006

Prostatectomy patients' postoperative pain assessment in the recovery room.

J Adv Nurs 2005 Dec;52(6):592-600

Turku Polytechnic and Department of Nursing, University of Turku, Turku, Finland.

Aim: This paper reports a study to assess the usability and use of different pain assessment tools and to compare patients' and nurses' pain assessments in the recovery room after prostatectomy.

Background: Pain assessment is the first step towards providing adequate pain relief but poses problems because of the subjective nature of the pain experience and the lack of quantifiable measurements. Pain tools have been tested in several clinical settings, but not in the recovery room.

Methods: Data were collected in the recovery room from 45 consecutive patients who had undergone prostatectomy by asking them to evaluate their pain intensity using visual analogue scale, numeric rating scale and verbal expressions. One of two research nurses measured patients' pain at regular intervals and at the same time as the patients. Physiological parameters were also evaluated. Data were analysed as frequencies and percentages. Sum variables were formed and results were analysed using Spearman's rank correlation, Pearson's correlation and with multiple regression analysis.

Results: Patients varied in their ability to assess the intensity of their pain using different tools, but assessments were correlated with each other and with nurses' estimations. Nurses and patients obtained similar assessments, but nurses both underestimated and overestimated patients' pain. Patients' verbal assessments varied widely. Patients' and nurses' pain assessments showed no association with patients' pulse or mean arterial blood pressure.

Conclusions: According to our results, it is not totally clear whether pain tools are usable in the recovery room. This issue calls for further research.
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http://dx.doi.org/10.1111/j.1365-2648.2005.03631.xDOI Listing
December 2005