Publications by authors named "Victoria Novik"

6 Publications

  • Page 1 of 1

Effect of high and low glycemic index breakfast on postprandial metabolic parameters and satiety in subjects with type 2 diabetes mellitus under intensive insulin therapy: Controlled clinical trial.

Clin Nutr ESPEN 2017 Aug 11;20:12-16. Epub 2017 May 11.

Universidad de Chile, Chile. Electronic address:

Background And Aim: The results of studies evaluating the metabolic effects of glycemic index (GI) in subjects with type 2 diabetes mellitus (DM2) have been contradictory. Consequently, the benefits of its application are controversial and polarized opinions of international organizations have been disclosed. The above situation leads this study to evaluate the acute effect of low and high GI breakfast on the glycemic response and satiety in subjects with DM2 under intensive insulin therapy (IIT).

Methods: A controlled, crossover and single-blind clinical trial was developed involving 10 obese subjects with DM2 under IIT, with a period of at least six months under IIT and with fast insulin prescription before breakfast. Subjects ingested on two different occasions a high or low GI breakfast. In both stages, glycemia was evaluated at 0 (basal), 30, 60 and 120 min, and satiety and satiation were evaluated through a visual analogue scale.

Results: In contrast to high GI breakfast, the low GI meal generated a significant decrease of 46% for the area under the curve of glucose (Δ 1940 mg/dL × 120 min, p = 0.022) and in mean glycemia evaluated at 30, 60 and 120 min. Moreover, in the low GI stage 8 of 10 patients achieved a 2 h postprandial glycemia lower than 180 mg/dL, without statistical significance. A nonsignificant increase of 12.7% (Δ 1.06 cm, p = 0.271) in satiety at 120 min in the low GI stage was observed.

Conclusion: In contrast to high GI breakfast, the low GI breakfast generated a significantly lower glycemic response. This assay allowed for the contribution of more in depth nutritional recommendations for this group of patients. Registered under ClinicalTrials.gov Identifier no. NCT02881164.
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http://dx.doi.org/10.1016/j.clnesp.2017.04.082DOI Listing
August 2017

[Erectile dysfunction among diabetic patients].

Authors:
Victoria Novik

Rev Med Chil 2014 Jun;142(6):809

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http://dx.doi.org/10.4067/S0034-98872014000600020DOI Listing
June 2014

Cell-Type-Specific Effects of Silibinin on Vitamin D-Induced Differentiation of Acute Myeloid Leukemia Cells Are Associated with Differential Modulation of RXRα Levels.

Leuk Res Treatment 2012 20;2012:401784. Epub 2012 May 20.

Department of Clinical Biochemistry, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, 84105 Beer-Sheva, Israel.

Plant polyphenols have been shown to enhance the differentiation of acute myeloid leukemia (AML) cells induced by the hormonal form of vitamin D(3) (1α,25-dihydroxyvitamin D(3); 1,25D). However, how these agents modulate 1,25D effects in different subtypes of AML cells remains poorly understood. Here, we show that both carnosic acid (CA) and silibinin (SIL) synergistically enhancd 1,25D-induced differentiation of myeloblastic HL60 cells. However, in promonocytic U937 cells, only CA caused potentiation while SIL attenuated 1,25D effect. The enhanced effect of 1,25D+CA was accompanied by increases in both the vitamin D receptor (VDR) and retinoid X receptor alpha (RXRα) protein levels and vitamin D response element (VDRE) transactivation in both cell lines. Similar increases were observed in HL60 cells treated with 1,25D + SIL. In U937 cells, however, SIL inhibited 1,25D-induced VDRE transactivation concomitant with downregulation of RXRα at both transcriptional and posttranscriptional levels. These inhibitory effects correlated with the inability of SIL, with or without 1,25D, to activate the Nrf2/antioxidant response element signaling pathway in U937 cells. These results suggest that opposite effects of SIL on 1,25D-induced differentiation of HL60 and U937 cells may be determined by cell-type-specific signaling and transcriptional responses to this polyphenol resulting in differential modulation of RXRα expression.
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http://dx.doi.org/10.1155/2012/401784DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505927PMC
December 2012

The Nrf2 transcription factor is a positive regulator of myeloid differentiation of acute myeloid leukemia cells.

Cancer Biol Ther 2011 Feb 1;11(3):317-29. Epub 2011 Feb 1.

Department of Clinical Biochemistry, Faculty of Health Sciences, Ben-Gurion University of the Negev, Petakh Tikva, Israel.

1α,25-dihydroxyvitamin D3 (1,25D) is a powerful differentiation agent, which has potential for treatment of acute myeloid leukemia (AML), but induces severe hypercalcemia at pharmacologically active doses. We have previously shown that carnosic acid (CA), the polyphenolic antioxidant from rosemary plant, markedly potentiates differentiation induced by low concentrations of 1,25D in human AML cell lines. Here, we demonstrated similar enhanced differentiation responses to the 1,25D/CA combination in primary leukemic cells derived from patients with AML, and determined the role of the Nrf2/antioxidant response element (Nrf2/ARE) pathway in these effects using U937 human monoblastic leukemia cells as the model. CA strongly transactivated the ARE-luciferase reporter gene, induced the ARE-responsive genes, NADP(H)-quinone oxidoreductase and the γ-glutamylcysteine synthetase heavy subunit, and elevated cellular glutathione levels. Interestingly, 1,25D potentiated the effects of CA on these activities. Stable transfection of wild-type (wt) Nrf2 resulted in the enhancement, while transfection of dominant-negative (dn) Nrf2 produced suppression of differentiation induced by the 1,25D/CA combination and, surprisingly, by 1,25D alone. These opposite effects were associated with a corresponding increase or decrease in vitamin D receptor and retinoid X receptor-α protein levels, and in vitamin D responsive element transactivation. Cells transfected with wtNrf2 and dnNrf2 also displayed opposing changes in the levels of the AP-1 family proteins (c-Jun and ATF2) and AP-1 transcriptional activity. Pretreatment with AP-1 decoy oligodeoxynucleotide markedly attenuated the differentiation in wtNrf2-transfected cells, suggesting that the pro-differentiation action of Nrf2 is mediated by functional AP-1. Our findings suggest that the Nrf2/ARE pathway plays an important part in the cooperative induction of myeloid leukemia cell differentiation by 1,25D and a plant polyphenol.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047086PMC
http://dx.doi.org/10.4161/cbt.11.3.14098DOI Listing
February 2011

Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D(3).

Cell Cycle 2010 Nov 15;9(22):4542-51. Epub 2010 Nov 15.

Department of Pathology and Laboratory Medicine, New Jersey Medical School, University of Medicine and Dentistry New Jersey, Newark, USA.

Acute myelogenous leukemia (AML) is a disease characterized by dysregulated cell proliferation associated with impaired cell differentiation, and current treatment regimens rarely save the patient. Thus, new mechanism-based approaches are needed to improve prognosis of this disease. We have investigated in preclinical studies the potential anti-leukemia use of the plant-derived polyphenol Silibinin (SIL) in combination with 1,25-dihydroxyvitamin D3 (1,25D). Although most of the leukemic blasts ex vivo responded by differentiation to treatment with this combination, the reasons for the absence of SIL-1,25D synergy in some cases were unclear. Here we report that failure of SIL to enhance the action of 1,25D is likely due to the SIL-induced increase in the activity of differentiation-antagonizing cell components, such as ERK5. This kinase is under the control of Cot1/Tlp2, and inhibition of Cot1 activity by a specific pharmacological inhibitor 4-(3-chloro-4-fluorophenylamino)-6-(pyridin-3-yl-methylamino-3-cyano-[1-7]-naphthyridine, or by Cot1 siRNA, increases the differentiation by SIL/1,25D combinations. Conversely, over-expression of a Cot1 construct increases the cellular levels of P-ERK5, and SIL/1,25D-induced differentiation and cell cycle arrest are diminished. It appears that reduction in ERK5 activity by inhibition of Cot1 allows SIL to augment the expression of 1,25D-induced differentiation promoting factors and cell cycle regulators such as p27 (Kip1) , which leads to cell cycle arrest. This study shows that in some cell contexts SIL/1,25D can promote expression of both differentiation-promoting and differentiation-inhibiting genes, and that the latter can be neutralized by a highly specific pharmacological inhibitor, suggesting a potential for supplementing treatment of AML with this combination of agents.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3048050PMC
http://dx.doi.org/10.4161/cc.9.22.13790DOI Listing
November 2010

[Global respiratory failure as the presentation form of hypothyroidism. Report of one case].

Rev Med Chil 2004 Jan;132(1):81-4

Departamento de Endocrinología, Servicio de Medicina del Hospital Dr. Gustavo Fricke de Viña del Mar.

We report a 36 years male, admitted to the hospital for progressive respiratory failure. Chest X ray and CT scan were normal. On admission, a severe bradycardia and slow intellectual activity were noted. Serum thyroid function tests showed a TSH over 150 microU/ml and T3 of 75 ng/ml. Thyroid substitution therapy was associated with a progressive improvement of respiratory function. Diaphragmatic dysfunction, central hypoventilation, airway obstruction, sleep apnea and pleural effusion have been previously reported in patients with hypothyroidism. Therefore, we recommend to measure TSH in patients with unexplained respiratory failure.
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http://dx.doi.org/10.4067/s0034-98872004000100013DOI Listing
January 2004
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