Grape products have been known to exert greater antioxidant and anti-obesity than anti-hyperglycemic effects in animals and humans. Omija is used as an ingredient in traditional medicine, and it is known to have an anti-hyperglycemic effect. We investigated whether the combined extracts of grape pomace and omija fruit (GE+OE) could reduce fat accumulation in adipose and hepatic tissues and provide beneficial effects against hyperglycemia and insulin resistance in type 2 diabetic mice. C57BL/KsJ-db/db mice were fed either a normal control diet or GE+OE (0.5% grape pomace extract and 0.05% omija fruit extract, w/w) for 7 weeks. GE+OE decreased plasma leptin and resistin levels while increasing adiponectin levels and reducing the total white adipose tissue weight. Furthermore, GE+OE lowered plasma free fatty acid (FFA), triglyceride, and total-cholesterol levels as well as hepatic FFA and cholesterol levels. Hepatic fatty acid synthase and glucose 6-phosphate dehydrogenase activities were decreased in the GE+OE group, whereas hepatic ${\beta}$-oxidation activity was increased. Furthermore, GE+OE supplementation not only reduced hyperglycemia and pancreatic ${\beta}$-cell failure but also lowered blood glycosylated hemoglobin and plasma insulin levels. The homeostasis model assessment of insulin resistance levels was also decreased and the decrease seems to be mediated by the lowered activities of hepatic glucose-6-phosphatase and phosphoenolpyruvate carboxykinases. The present data suggest that GE+OE may have the potential to reduce hyperglycemia, insulin resistance, and obesity in patients with type 2 diabetes.
BACKGROUND/OBJECTIVES: Vitamin D plays an important role in the etiology of gestational diabetes mellitus (GDM). This study evaluated the effect of vitamin D supplementation on metabolic indices and hs-C-reactive protein (CRP) levels in GDM patients. SUBJECTS/METHODS: The study was a randomized, placebo-controlled, double-blinded clinical trial. Seventy-six pregnant women with GDM and gestational age between 24-28 weeks were assigned to receive four oral treatments consisting of 50,000 IU of vitamin $D_3$ (n = 38) or placebo (n = 38) once every 2 weeks for 2 months. Fasting blood glucose (FG), insulin, HbA1c, 25-hydroxyvitamin D, lipid profile, hs-CRP, and homeostasis model assessment-insulin resistance (HOMA-IR) were measured before and after treatment. Independent and paired t-tests were used to determine intra- and intergroup differences, respectively. ANCOVA was used to assess the effects of vitamin D supplementation on biochemical parameters. RESULTS: Compared with the placebo group, in the vitamin D group, the serum level of 25-hydroxyvitamin D increased (19.15 vs. -0.40 ng/ml; P < 0.01) and that of FG (-4.72 vs. 5.27 mg/dl; P = 0.01) as well as HbA1c (-0.18% vs. 0.17%; P = 0.02) decreased. Improvements in the lipid profiles were observed in the vitamin D group, but without statistical significance. Significant increases in concentrations of hs-CRP, FG, HbA1c, total cholesterol, and LDL cholesterol were observed in the placebo group. No significant change in fasting insulin and HOMA-IR was observed in either group. CONCLUSIONS: In GDM patients, vitamin D supplementation improved FG and HbA1c but had no significant effects on lipid profile or hs-CRP.
Zinc deficiency is known to be associated with insulin resistance in obese individuals. This study was performed to evaluate the effect of zinc supplementation on insulin resistance and metabolic risk factors in obese Korean women. Forty obese women (body mass index (BMI) ${\geq}25kg/m^2$) aged 19-28 years were recruited for this study. Twenty women of the study group took 30 mg/day of supplemental zinc as zinc gluconate for 8 weeks and 20 women of control group took placebo. Usual dietary zinc intake was estimated from 3-day diet records. Insulin resistances were measured using Homeostasis model assessment (HOMA) indices, and insulin sensitivities Matsuda indices, which were calculated using oral glucose tolerance test data. Metabolic risk factors, such as waist circumference, blood pressure, fasting glucose, triglyceride, high density lipoprotein (HDL) cholesterol, and adipocyte hormones such as leptin, and adiponectin were also measured. At the beginning of study, dietary zinc averaged 7.31 mg/day and serum zinc averaged $12.98{\mu}mol/L$ in the study group. Zinc supplementation increased serum zinc by 15% and urinary zinc by 56% (P < 0.05). HOMA values tended to decrease and insulin sensitivity increased slightly in the study group, but not significantly so. BMI, waist circumference, blood pressure, blood glucose, triglyceride, HDL cholesterol, and adipocyte hormones did not change in either the study or control group. These results suggest that zinc status may not affect insulin resistance and metabolic risk factors in obese Korean women. Further research is required on a larger cohort with a longer follow-up to determine the effects of zinc status on insulin resistance and metabolic variables.
This study investigated the hypoglycemic, hypolipidemic, and antioxidant effects of dietary quercetin in an animal model of type 2 diabetes mellitus. Four-week-old C57BL/KsJ-db/db mice (n = 18) were offered an AIN-93G diet or a diet containing quercetin at 0.04% (low quercetin, LQE) or 0.08% of the diet (high quercetin, HQE) for 6 weeks after 1 week of adaptation. Plasma glucose, insulin, adiponectin, and lipid profiles, and lipid peroxidation of the liver were determined. Plasma glucose levels were significantly lower in the LQE group than in the control group, and those in the HQE group were even further reduced compared with the LQE group. The homeostasis model assessment for insulin resistance (HOMA-IR) showed lower values for LQE and HQE than for the control group without significant influence on insulin levels. High quercetin increased plasma adiponectin compared with the control group. Plasma triglycerides in the LQE and HQE groups were lower than those in the control group. Supplementation with high quercetin decreased plasma total cholesterol and increased HDL-cholesterol compared with the control group. Consumption of low and high quercetin reduced thiobarbituric acid reactive substances (TBARS) levels and elevated activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver. Thus, quercetin could be effective in improving hyperglycemia, dyslipidemia, and antioxidant status in type 2 diabetes.
Chronic consumption of a high-fat, high-sucrose (HFHS) diet increases insulin resistance and results in type 2 diabetes mellitus in C57BL/6J mice. Hyperglycemia in diabetics increases oxidative stress, which is associated with a high risk of diabetic complications. The purpose of this study was to examine the hypoglycemic and antioxidant effects of chamnamul [Pimpinella brachycarpa (Kom.) Nakai] in an animal model of type 2 diabetes. The ${\alpha}$-glucosidase inhibitory activity of a 70% ethanol extract of chamnamul was measured in vitro. Five-week-old male C57BL/6J mice were fed a basal or HFHS diet with or without a 70% ethanol extract of chamnamul at a 0.5% level of the diet for 12 weeks after 1 week of adaptation. After sacrifice, serum glucose, insulin, adiponectin, and lipid profiles, and lipid peroxidation of the liver were determined. Homeostasis model assessment for insulin resistance (HOMA-IR) was determined. Chamnamul extract inhibited ${\alpha}$-glucosidase by 26.7%, which was 78.3% the strength of inhibition by acarbose at a concentration of 0.5 mg/mL. Serum glucose, insulin, and cholesterol levels, as well as HOMA-IR values, were significantly lower in the chamnamul group than in the HFHS group. Chamnamul extract significantly decreased the level of thiobarbituric acid reactive substances and increased the activities of superoxide dismutase, catalase, and glutathione peroxidase in the liver compared with the HFHS group. These findings suggest that chamnamul may be useful in prevention of hyperglycemia and reduction of oxidative stress in mice fed a HFHS diet.
Purpose: The rising prevalence of childhood obesity in the past decades has caused non-alcoholic fatty liver disease (NAFLD) to become the most common cause of pediatric chronic liver disease worldwide. This study was aimed at determining the effect of vitamin D (Vit D) on ultrasonography and laboratory indices of NAFLD and some blood biochemical indicators in children. Methods: In this interventional study liver ultrasonography was performed in 200 children with overweight and obesity. A 108 had fatty liver among which 101 were randomly divided into two groups of study (n=51) and control (n=50). The study group was treated with Vit D, 50000 U once a week whereas the control group received placebo with the same dose and package, both for 12 weeks. At the end of the intervention lab tests and ultrasound study was performed once again to evaluate the response to treatment. Results: It was found out that Vit D supplementation improved the fatty liver grade in the study group. The mean changes in hemoglobin (Hb), uric acid, highdensity lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), insulin, albumin and alanine aminotransferase (ALT) was significantly higher in the study group compared to controls (p<0.05). After the intervention and means adjustment, a significant difference was obtained in HDL-C, insulin, LDL-C and homeostasis model assessment of insulin resistance (HOMA-IR) between the two groups. Conclusion: Vit D supplementation in addition to improving the fatty liver grade in ultrasonography and increasing the blood Vit D level, increases the HDL and Hb level besides decreasing uric acid, LDL, HOMA-IR, insulin and ALT levels.
Protein tyrosine phosphatase 1B (PTP1B) is important in the regulation of metabolic diseases and has emerged as a promising signaling target. Previously, we reported the PTP1B inhibitory activity of Rheum undulatum (RU). In the present study, we investigated the metabolic regulatory effects of RU in a high-fat diet (HFD) model. RU treatment significantly blocked body weight gain, which was accompanied by a reduction of feed efficiency. In addition, it led to a reduction of liver weight mediated by overexpression of PPAR${\alpha}$ and CPT1 in the liver, and an increase in the expression of adiponectin, aP2, and UCP3 in adipose tissue responsible for the reduction of total and LDL-cholesterol levels. Chrysophanol and physcion from RU significantly inhibited PTP1B activity and strongly enhanced insulin sensitivity. Altogether, our findings strongly suggest that 2 compounds are novel PTP1B inhibitors and might be considered as anti-obesity agents that are effective for suppressing body weight gain and improving lipid homeostasis.
Background: Subclinical hypothyroidism (SH) is a common condition in obese children. However, its effect on glucose and lipid metabolism in obese children remains controversial. Purpose: The present study aimed to investigate the association between SH and metabolic parameters. Methods: A total of 215 obese children and adolescents aged 6-18 years were included in this retrospective cross-sectional study. The patients' anthropometric measurements such as thyrotropin (TSH), free thyroxine (fT4), fasting plasma glucose, and insulin levels, as well as homeostasis model assessment for insulin resistance (HOMA-IR) index, and lipid profiles were evaluated. The patients were allocated to the SH group (fT4 normal, TSH 5-10 mIU/L) (n=77) or the control group (fT4 normal, TSH<5 mIU/L) (n=138). The glucose and lipid metabolisms of the 2 groups were compared. Results: SH was identified in 77 of 215 patients (36%). Mean body mass index was similar in both groups. The mean serum insulin, HOMA-IR, and triglyceride (TG) levels were higher and the mean high-density lipoprotein cholesterol level was lower in the SH group than in the control group (P=0.007, P=0.004, P=0.01, and P=0.02, respectively). A positive correlation was observed between TSH level and insulin level, HOMA-IR, and TG level. Conclusion: SH was identified in some of the obese children and adolescents. A clear association was observed between SH, insulin resistance, and dyslipidemia in obese children.
Verit, Fatma Ferda;Zeyrek, Fadile Yildiz;Zebitay, Ali Galip;Akyol, Hurkan
Clinical and Experimental Reproductive Medicine
/
v.44
no.1
/
pp.28-32
/
2017
Objective: Growing evidence suggests that increased cardiovascular disease (CVD) risk is associated with female infertility caused by conditions such as polycystic ovarian disease, obesity, thyroid dysfunction, and endometriosis. The aim of this study was to evaluate whether any relationship exists between CVD and unexplained infertility. Methods: Sixty-five women with unexplained infertility and 65 fertile controls were enrolled in the study. CVD risk markers such as low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), triglycerides (TG), insulin resistance (defined by the homeostasis model assessment ratio), and high-sensitivity C-reactive protein (hs-CRP) were assessed. Results: TG, TC, LDL, and hs-CRP levels were higher and HDL levels were lower in patients with unexplained infertility than in fertile controls (p<0.05 for all). Positive associations were found between unexplained infertility and TG, TC, LDL, and hs-CRP levels, and a negative correlation was found for HDL (p<0.05 for all). Multivariate logistic regression analysis showed that TG, HDL, and hs-CRP were independent variables associated with unexplained infertility. Conclusion: Our study showed that women with unexplained infertility had an atherogenic lipid profile and elevated hs-CRP levels, suggesting a higher risk of developing CVD in the future. Further studies with larger groups are needed to investigate the nature of this link.
Journal of the Korean Society of Food Science and Nutrition
/
v.20
no.2
/
pp.187-196
/
1991
Aging is the progressive accumulation of changes with time associated with responsible for the ever-increasing susceptibility to disease and death which accompanies advancing age. Lipid peroxides easily produced in the membrane system by the chain reaction of free radicals which occurred from various environmental factors. The amount of lipid peroxides produced in biological system increased with aging process, and lipid peroxidation damages involved in aging process and pathological disorders. Although lipid peroxides have such deleterious effects on the organisms, there are numerous substances and mechanisms which prevent the reaction of peroxide formation and protect the subject from its toxicity. This review provides an overview of how does lipid peroxidation of unsaturated lipids take place by free radical, and what is the intervention of lipid peroxides in pathogenesis of some human diseases, and also how does food restriction influences the aging process and various pathological disorders. The major focus of this paper is to review the evidence indicating that food restriction retards the aging process, and possible mechanisms of its actions. Therefore, it discussed the effects of age and food restriction on life-span, membrane yield, lipid peroxidation, fatty acid composition and peroxidizability, cholesterol and triglyceride levels, prostaglasndin and thromboxane synthesis, which may be concerned with blood flow, membrane fluidity, homeostasis and glomerular filtration rate in living body.
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