Comparative assessment of estrogenic responses with relevance to the metabolic syndrome and to menopausal symptoms in wild-type and aromatase-knockout mice

Niacin (nicotinic acid) has recently been shown to increase serum adiponectin concentrations in men with the metabolic syndrome. However, little is known about the mechanism(s) by which niacin regulates the intracellular trafficking and secretion of adiponectin. Since niacin appears to exert its effects on lipolysis through receptor (GPR109A)-dependent and -independent pathways, the purpose of this investigation was to examine the role of the recently identified GPR109A receptor in adiponectin secretion. Initial in vivo studies in rats demonstrated that niacin (30 mg/kg po) acutely increases serum adiponectin concentrations, whereas it decreases NEFAs. Further in vitro studies demonstrated an increase in adiponectin secretion and a decrease in lipolysis in primary adipocytes following treatment with niacin or β-hydroxybutyrate (an endogenous ligand of the GPR109A receptor), but these effects were blocked when adipocytes were pretreated with pertussis toxin. Niacin had no effect on adiponectin secretion or lipolysis in 3T3-L1 adipocytes, which have limited cell surface expression of the GPR109A receptor. To further substantiate these in vitro findings, wild-type and GPR109A receptor knockout mice were administered a single dose of niacin or placebo, and serum was obtained for the determination of adiponectin and NEFA concentrations. Serum adiponectin concentrations increased and serum NEFAs decreased in the wild-type mice within 10 min following niacin administration. However, niacin administration had no effect on adiponectin and NEFA concentrations in the GPR109A receptor knockout mice. These results demonstrate that the GPR109A receptor plays an important role in the dual regulation of adiponectin secretion and lipolysis.

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Evaluation of the presence and severity of menopausal symptoms among postmenopausal women screened for the metabolic syndrome

Gynecological Endocrinology ◽

10.3109/09513590.2014.971236 ◽

2014 ◽

Vol 30 (12) ◽

pp. 918-924 ◽

Cited By ~ 3

Author(s):

Peter Chedraui ◽

Faustino R. Pérez-López ◽

Luis Hidalgo ◽

Diego Villacreses ◽

Andrea Domínguez ◽

...

Keyword(s):

Metabolic Syndrome ◽

Postmenopausal Women ◽

Menopausal Symptoms ◽

The Metabolic Syndrome

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Deficiency of intestinal mucin-2 protects mice from diet-induced fatty liver disease and obesity

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00094.2015 ◽

2016 ◽

Vol 310 (5) ◽

pp. G310-G322 ◽

Cited By ~ 17

Author(s):

Phillipp Hartmann ◽

Caroline T. Seebauer ◽

Magdalena Mazagova ◽

Angela Horvath ◽

Lirui Wang ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Knockout Mice ◽

Fatty Liver Disease ◽

Mucus Layer ◽

Wild Type ◽

Intestinal Mucus ◽

The Metabolic Syndrome ◽

Mucin 2 ◽

Intestinal Mucus Layer

Nonalcoholic fatty liver disease (NAFLD) and obesity are characterized by altered gut microbiota, inflammation, and gut barrier dysfunction. Here, we investigated the role of mucin-2 (Muc2) as the major component of the intestinal mucus layer in the development of fatty liver disease and obesity. We studied experimental fatty liver disease and obesity induced by feeding wild-type and Muc2-knockout mice a high-fat diet (HFD) for 16 wk. Muc2 deficiency protected mice from HFD-induced fatty liver disease and obesity. Compared with wild-type mice, after a 16-wk HFD, Muc2-knockout mice exhibited better glucose homeostasis, reduced inflammation, and upregulated expression of genes involved in lipolysis and fatty acid β-oxidation in white adipose tissue. Compared with wild-type mice that were fed the HFD as well, Muc2-knockout mice also displayed higher intestinal and plasma levels of IL-22 and higher intestinal levels of the IL-22 target genes Reg3b and Reg3g. Our findings indicate that absence of the intestinal mucus layer activates the mucosal immune system. Higher IL-22 levels protect mice from diet-induced features of the metabolic syndrome.

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Association of polimorphism rs1801282 with different components of the metabolic syndrome

HERALD of North-Western State Medical University named after I I Mechnikov ◽

10.17816/mechnikov201810239-43 ◽

2018 ◽

Vol 10 (2) ◽

pp. 39-43

Author(s):

T V Eremenko ◽

S M Kotova ◽

I Yu Matezius ◽

F K Khetagurova ◽

F M Radugin

Keyword(s):

Metabolic Syndrome ◽

Clinical Laboratory ◽

High Density Lipoproteins ◽

Newly Diagnosed ◽

Wild Type ◽

The Metabolic Syndrome ◽

Medical University ◽

Instrumental Methods ◽

Pparγ Gene ◽

North Western

Objective. To study the association of polymorphism rs1801282 of the PPARγ gene with different components of metabolic syndrome (MS). Materials and methods. 145 subjects with newly diagnosed MS were examined. All subjects underwent a clinical examination, including general clinical, laboratory and instrumental methods; presence of polymorphism rs1801282 of the PPARγ gene was also determined. Results. In the group of subjects with rs1801282 polymorphism, hyperglycemia was observed less frequently compared with the rest of subjects the incidence was 53.8% and 79.8% cases respectively (p = 0.005). A decrease in the risk of arterial hypertension was also observed in subjects with polymorphic allele: an increase in blood pressure was noted in 70.6% of rs1801282 group and 96.2% for wild type PPARγ (p < 0.001) When analyzing levels of triglycerides and high-density lipoproteins, an increase in these parameters was noted in the group of subjects with rs1801282 polymorphism. Conclusion. The results of the study indicate the association of rs1801282 polymorphism in subjects with metabolic syndrome with a number of clinical features of the disease, dyslipidemia and a reduction of the risk of hyperglycemia and hypertension. (For citation: Eremenko TV, Kotova SM, Matezius IYu, et al. Association of polimorphism rs1801282 with different components of the metabolic syndrome. Herald of North-Western State Medical University named after I.I. Mechnikov. 2018;10(2):39-43. doi: 10.17816/mechnikov201810239-43).

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Association of polimorphism rs1801282 with different components of the metabolic syndrome

HERALD of North-Western State Medical University named after I I Mechnikov ◽

10.17816/mechnikov201810360-64 ◽

2018 ◽

Vol 10 (3) ◽

pp. 60-64

Author(s):

Tatiana V. Eremenko

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Arterial Hypertension ◽

Clinical Laboratory ◽

High Density Lipoproteins ◽

Newly Diagnosed ◽

Wild Type ◽

The Metabolic Syndrome ◽

Instrumental Methods ◽

Pparγ Gene

Objective. To study the association of polymorphism rs1801282 of the PPARγ gene with different components of metabolic syndrome (MS). Materials and methods. 145 subjects with newly diagnosed MS were examined. All subjects underwent a clinical examination, including general clinical, laboratory and instrumental methods; presence of polymorphism rs1801282 of the PPARγ gene was also determined. Results. In the group of subjects with rs1801282 polymorphism, hyperglycemia was observed less frequently compared with the rest of subjects the incidence was 53.8% and 79.8% cases respectively (p = 0.005). A decrease in the risk of arterial hypertension was also observed in subjects with polymorphic allele: an increase in blood pressure was noted in 70.6% of rs1801282 group and 96.2% for wild type PPARγ (p < 0.001). When analyzing levels of triglycerides and high-density lipoproteins, an increase in these parameters was noted in the group of subjects with rs1801282 polymorphism. Conclusion. The results of the study indicate the association of rs1801282 polymorphism in subjects with metabolic syndrome with a number of clinical features of the disease, dyslipidemia and a reduction of the risk of hyperglycemia and hypertension.

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A variant in the heart-specific fatty acid transport protein 6 is associated with lower fasting and postprandial TAG, blood pressure and left ventricular hypertrophy

British Journal Of Nutrition ◽

10.1017/s0007114511004727 ◽

2011 ◽

Vol 107 (10) ◽

pp. 1422-1428 ◽

Cited By ~ 6

Author(s):

Annegret Auinger ◽

Ulf Helwig ◽

Maria Pfeuffer ◽

Diana Rubin ◽

Mark Luedde ◽

...

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Fatty Acid ◽

Left Ventricular ◽

Transport Protein ◽

Fatty Acid Transport ◽

Acid Transport ◽

Wild Type ◽

Fatty Acid Transport Protein ◽

The Metabolic Syndrome

Fatty acid transport protein 6 (FATP6) is primarily expressed in the heart and seems to be involved in cardiac fatty acid uptake. Therefore, we investigated whether a variation in the 5′-untranslated region of the FATP6 gene is associated with features of the metabolic syndrome and signs of myocardial alteration or heart failure. A total of 755 male participants from a Metabolic Intervention Cohort Kiel were genotyped for the FATP6–7T>A polymorphism (rs2526246) and phenotyped for features of the metabolic syndrome. Participants underwent a glucose tolerance test and the postprandial assessment of metabolic variables after a standardised mixed meal. Left ventricular heart function was evaluated in fifty-four participants. Fasting (P = 0·01) and postprandial (P = 0·02) TAG concentrations were significantly lower in AA homozygotes when compared with wild-type carriers. Homozygosity of allele A was associated with significantly lower postprandial insulin concentrations after a glucose load and significantly lower systolic (P = 0·01) and diastolic (P = 0·01) blood pressure values compared with wild-type carriers. Accordingly, left ventricular heart mass was significantly lower in twenty-seven AA homozygotes in comparison with twenty-seven TT homozygotes, matched for BMI (P = 0·04). In conclusion, the effects of the FATP6 polymorphism on TAG are mediated by affluent dietary fat. The FATP6–7T>A polymorphism may protect from traits of the metabolic syndrome and CVD.

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