Green and Black Tea Suppress Hyperglycemia and Insulin Resistance by Retaining the Expression of Glucose Transporter 4 in Muscle of High-Fat Diet-Fed C57BL/6J Mice

2010 ◽  
Vol 58 (24) ◽  
pp. 12916-12923 ◽  
Author(s):  
Shin Nishiumi ◽  
Hiroaki Bessyo ◽  
Mayuko Kubo ◽  
Yukiko Aoki ◽  
Akihito Tanaka ◽  
...  
Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1829 ◽  
Author(s):  
Lepore ◽  
Maggisano ◽  
Bulotta ◽  
Mignogna ◽  
Arcidiacono ◽  
...  

Oleacein is one of the most abundant polyphenolic compounds of olive oil, which has been shown to play a protective role against several metabolic abnormalities, including dyslipidemia, insulin resistance, and glucose intolerance. Herein, we investigated the effects of oleacein on certain markers of adipogenesis and insulin-resistance in vitro, in 3T3-L1 adipocytes, and in vivo in high-fat diet (HFD)-fed mice. During the differentiation process of 3T3-L1 preadipocytes into adipocytes, oleacein strongly inhibited lipid accumulation, and decreased protein levels of peroxisome proliferator-activated receptor gamma (PPARγ) and fatty acid synthase (FAS), while increasing Adiponectin levels. In vivo, treatment with oleacein of C57BL/6JOlaHsd mice fed with HFD for 5 and 13 weeks prevented the increase in adipocyte size and reduced the inflammatory infiltration of macrophages and lymphocytes in adipose tissue. These effects were accompanied by changes in the expression of adipose tissue-specific regulatory elements such as PPARγ, FAS, sterol regulatory element-binding transcription factor-1 (SREBP-1), and Adiponectin, while the expression of insulin-sensitive muscle/fat glucose transporter Glut-4 was restored in HFD-fed mice treated with oleacein. Collectively, our findings indicate that protection against HFD-induced adiposity by oleacein in mice is mediated by the modulation of regulators of adipogenesis. Protection against HFD-induced obesity is effective in improving peripheral insulin sensitivity.


2019 ◽  
Vol 8 ◽  
Author(s):  
Kübra Akalın ◽  
Arzu Taş Ekiz ◽  
Fatih Karakaya ◽  
Ayse Karadag ◽  
Ebru Pelvan ◽  
...  

Type-2 diabetes (T2D) is the most common type of chronic disease in adults and accounts for around 90% of all cases of diabetes. Therefore, developing dietary supplements from natural sources, such as teas, is of great interest. Seven diet groups together with a parallel control group were used for three periods of 16 weeks in total [stabilization period (W-2-W0), model period (W0-W8), and treatment period (W8-W14)]. The primary aim of this study was to investigate the in vivo antidiabetic activities of green and black tea polysaccharides (GTPS and BTPS, respectively) using streptozotocin induced diabetic mice fed with either a high-fat diet (HFD) or normal diet (ND). Streptozotocin and HFD induced T2D in vivo model was developed during the model period (W0-W8) in C57BL/6J male mice. Both GTPS and BTPS groups were administrated for 6 weeks (daily 400 mg/kg body weight) by oral gavage throughout the treatment period (W8-W14). The results showed that BTPS group significantly (P < 0.05) decreased the fasting blood glucose level in diabetic mice even fed with a HFD and improved the insulin resistance. Similar effect was not obtained when GTPS group fed with a HFD. In addition, BTPS group fed with a HFD effectively suppressed the body weight gain despite high energy intake and was more successful than its GTPS counterpart group in healing pathologies of liver and affected plasma blood lipid levels due to streptozotocin and HFD-induced diabetes. The present work suggests that BTPS can be used as an antidiabetic dietary supplement without posing any potential health risk.


Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 500-508 ◽  
Author(s):  
Li Chen ◽  
B. L. G. Nyomba

High-fat diet and intrauterine growth retardation may predispose to obesity, insulin resistance, and type 2 diabetes. Because prenatal ethanol (ETOH) exposure causes intrauterine growth retardation, we investigated its interactions with postnatal high-fat diet on glucose tolerance and adipocyte-derived hormones in the rat offspring. High-fat-fed offspring had increased adiposity, serum leptin, and muscle uncoupling protein-3, but decreased adiponectin mRNA, compared with corresponding chow-fed groups. ETOH-exposed offspring had normal adiponectin, but increased resistin mRNA and protein, compared with controls, regardless of postnatal diet. Skeletal muscle glucose transporter-4 content was decreased after both ETOH exposure and high-fat feeding. Glycemic and insulin responses to an ip glucose challenge were equally increased in non-ETOH-exposed high-fat-fed offspring and in ETOH-exposed chow-fed offspring, with additive effects of ETOH and high-fat diet. Pancreatic insulin content was elevated only in non-ETOH-exposed high-fat-fed offspring. The data suggest that high-fat diet worsens glucose intolerance in offspring of rats exposed to ETOH. Prenatal ETOH exposure and postnatal high-fat diet might cause insulin resistance through separate mechanisms, involving resistin and adiponectin, respectively.


2014 ◽  
Vol 18 (3) ◽  
pp. 197-203 ◽  
Author(s):  
Jinil Kim ◽  
Ja In Jeong ◽  
Kwang Min Kim ◽  
Inho Choi ◽  
Richard E. Pratley ◽  
...  

2010 ◽  
Vol 119 (6) ◽  
pp. 239-250 ◽  
Author(s):  
Vanessa Souza-Mello ◽  
Bianca M. Gregório ◽  
Fernando S. Cardoso-de-Lemos ◽  
Laís de Carvalho ◽  
Márcia B. Aguila ◽  
...  

The aim of the present study was to evaluate the effects of monotherapies and combinations of drugs on insulin sensitivity, adipose tissue morphology, and pancreatic and hepatic remodelling in C57BL/6 mice fed on a very HF (high-fat) diet. Male C57BL/6 mice were fed on an HF (60% lipids) diet or SC (standard chow; 10% lipids) diet for 10 weeks, after which time the following drug treatments began: HF-T (HF diet treated with telmisartan; 5.2 mg·kg−1 of body weight·day−1), HF-S (HF diet treated with sitagliptin; 1.08 g·kg−1 of body weight·day−1), HF-M (HF diet treated with metformin; 310.0 mg·kg−1 of body weight·day−1), HF-TM (HF diet treated with telmisartan+metformin), HF-TS (HF diet treated with telmisartan+sitagliptin) and HF-SM (HF diet treated with sitagliptin+metformin). Treated groups also had free access to the HF diet, and treatments lasted for 6 weeks. Morphometry, stereological tools, immunostaining, ELISA, Western blot analysis and electron microscopy were used. The HF diet yielded an overweight phenotype, an increase in oral glucose intolerance, hyperinsulinaemia, hypertrophied islets and adipocytes, stage 2 steatosis (>33%), and reduced liver PPAR-α (peroxisome-proliferator-activated receptor-α) and GLUT-2 (glucose transporter-2) levels, concomitant with enhanced SREBP-1 (sterol-regulatory-element-binding protein-1) expression (P<0.0001). Conversely, all drug treatments resulted in significant weight loss, a reversal of insulin resistance, islet and adipocyte hypertrophy, and alleviated hepatic steatosis. Only the HF-T and HF-TS groups had body weights similar to the SC group at the end of the experiment, and the latter treatment reversed hepatic steatosis. Increased PPAR-α immunostaining in parallel with higher GLUT-2 and reduced SREBP-1 expression may explain the favourable hepatic outcomes. Restoration of adipocyte size was consistent with higher adiponectin levels and lower TNF-α (tumour necrosis factor-α) levels (P<0.0001) in the drug-treated groups. In conclusion, all of the drug treatments were effective in controlling the metabolic syndrome. The best results were achieved using telmisartan and sitagliptin as monotherapies or as a dual treatment, combining partial PPAR-γ agonism and PPAR-α activation in the liver with extended incretin action.


Marine Drugs ◽  
2020 ◽  
Vol 18 (9) ◽  
pp. 483
Author(s):  
Shiwei Hu ◽  
Mengyu Du ◽  
Laijin Su ◽  
Huicheng Yang

Portunus trituberculatus eggs contain phospholipids, whose components and bioactivity are unclear. Here, we investigated the fatty acid composition of phosphatidylserine from P. trituberculatus eggs (Pt-PS). Moreover, its effects on insulin resistance and gut microbiota were also evaluated in high-fat-diet-fed mice. Our results showed that Pt-PS accounted for 26.51% of phospholipids and contained abundant polyunsaturated fatty acids (more than 50% of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)). Animal experiments indicated that Pt-PS significantly decreased body weight and adipose weight gain, improved hyperglycemia and hyperinsulinemia, mitigated insulin resistance, and regulated circulatory cytokines. Pt-PS activated insulin receptor substrate 1 (IRS1) and increased the levels of IRS1-associated phosphatidylinositol 3-hydroxy kinase (PI3K), phosphorylated protein kinase B (Akt) protein, and plasma membrane glucose transporter 4 protein. Furthermore, Pt-PS modified the gut microbiota, inducing, especially, a dramatic decrease in the ratio of Firmicutes to Bacteroidetes at the phylum level, as well as a remarkable improvement in their subordinate categories. Pt-PS also reduced fecal lipopolysaccharide concentration and enhanced fecal acetate, propionate, and butyrate concentrations. Additionally, the effects of Pt-PS on alleviation of insulin resistance and regulation of intestinal bacteria were better than those of phosphatidylserine from soybean. These results suggest that Pt-PS mitigates insulin resistance by altering the gut microbiota. Therefore, Pt-PS may be developed as an effective food supplement for the inhibition of insulin resistance and the regulation of human gut health.


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