scholarly journals Heat-killed and live Lactobacillus reuteri GMNL-263 exhibit similar effects on improving metabolic functions in high-fat diet-induced obese rats

2016 ◽  
Vol 7 (5) ◽  
pp. 2374-2388 ◽  
Author(s):  
Feng-Ching Hsieh ◽  
Cheng-Che E. Lan ◽  
Tsui-Yin Huang ◽  
Kuan-Wei Chen ◽  
Chee-Yin Chai ◽  
...  

Our objective was to investigate and compare the effects of heat-killed (HK) and liveLactobacillus reuteriGMNL-263 (Lr263) on insulin resistance and its related complications in high-fat diet (HFD)-induced rats.

2012 ◽  
Vol 18 (4) ◽  
pp. 262-268 ◽  
Author(s):  
Shu-yu Yang ◽  
Neng-jiang Zhao ◽  
Xue-jun Li ◽  
Hui-jie Zhang ◽  
Ke-ji Chen ◽  
...  

2010 ◽  
Vol 206 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Eliana H Akamine ◽  
Anderson C Marçal ◽  
João Paulo Camporez ◽  
Mara S Hoshida ◽  
Luciana C Caperuto ◽  
...  

Besides the effects on peripheral energy homeostasis, insulin also has an important role in ovarian function. Obesity has a negative effect on fertility, and may play a role in the development of the polycystic ovary syndrome in susceptible women. Since insulin resistance in the ovary could contribute to the impairment of reproductive function in obese women, we evaluated insulin signaling in the ovary of high-fat diet-induced obese rats. Female Wistar rats were submitted to a high-fat diet for 120 or 180 days, and the insulin signaling pathway in the ovary was evaluated by immunoprecipitation and immunoblotting. At the end of the diet period, we observed insulin resistance, hyperinsulinemia, an increase in progesterone serum levels, an extended estrus cycle, and altered ovarian morphology in obese female rats. Moreover, in female obese rats treated for 120 days with the high-fat diet, the increase in progesterone levels occurred together with enhancement of LH levels. The ovary from high-fat-fed female rats showed a reduction in the insulin receptor substrate/phosphatidylinositol 3-kinase/AKT intracellular pathway, associated with an increase in FOXO3a, IL1B, and TNFα protein expression. These changes in the insulin signaling pathway may have a role in the infertile state associated with obesity.


2012 ◽  
Vol 49 (1) ◽  
pp. 153-160 ◽  
Author(s):  
Sabrina Alves Lenquiste ◽  
Ângela Giovana Batista ◽  
Rafaela da Silva Marineli ◽  
Nathalia Romanelli Vicente Dragano ◽  
Mário Roberto Maróstica

2021 ◽  
Author(s):  
Minchun Zhang ◽  
Jie Chen ◽  
Minglan Yang ◽  
Cheng Qian ◽  
Yu Liu ◽  
...  

Abstract Background: Artificial sweeteners (AS) are widely used as sugar substitutes to reduce calorie intake. However, high doses of AS induced glucose tolerance by modulating gut microbiota. The objective of this study was to investigate the effects of lower doses of sucralose on fecal microbiota in obesity. Methods: Eight weeks after high-fat diet, the male Sprague Dawley rats were randomly divided into four groups (n=24) and administrated by a daily gavage of 2ml normal saline (CON), 0.54mM sucralose (N054), 0.78mM sucralose (N078) and 324mM sucrose (S324) respectively. After four weeks, fecal samples were obtained and used in 16S ribosomal RNA gene sequencing. Results: The richness and diversity of fecal microbiota did not change by these sucralose and sucrose dosage. Both 0.54mM (0.43mg) and 0.78mM (0.62mg) tended to reduce the beneficial bacteria, Lactobacillaceae and Akkermansiaceae. The relative abundance of family Acidaminoccaceae and its genus Phascolarctobacteriam were increased with 0.54mM sucralose. In functional prediction, 0.54mM sucralose increased profiles of carbohydrate metabolism, whereas 0.78 mM sucralose enhanced that of amino acids metabolism. Conclusions: The lower doses of sucralose altered the compositions and the metabolic functions of fecal microbiota. The benefits of sucralose and its recommended dose for obese patients should be reassessed comprehensively.


2021 ◽  
Vol 138 ◽  
pp. 111438
Author(s):  
Benjarat Janson ◽  
Janjira Prasomthong ◽  
Wachirawadee Malakul ◽  
Tantip Boonsong ◽  
Sakara Tunsophon

2017 ◽  
Vol 42 (8) ◽  
pp. 841-849 ◽  
Author(s):  
Sandhya Nair ◽  
Jacques Gagnon ◽  
Claude Pelletier ◽  
Nadia Tchoukanova ◽  
Junzeng Zhang ◽  
...  

Diet-induced obesity, insulin resistance, impaired glucose tolerance, chronic inflammation, and oxidative stress represent the main features of type 2 diabetes mellitus. The present study was conducted to examine the efficacy and mechanisms of shrimp oil on glucose homeostasis in obese rats. Male CD rats fed a high-fat diet (52 kcal% fat) and 20% fructose drinking water were divided into 4 groups and treated with the dietary replacement of 0%, 10%, 15%, or 20% of lard with shrimp oil for 10 weeks. Age-matched rats fed a low-fat diet (10 kcal% fat) were used as the normal control. Rats on the high-fat diet showed impaired (p < 0.05) glucose tolerance and insulin resistance compared with rats fed the low-fat diet. Shrimp oil improved (p < 0.05) oral glucose tolerance, insulin response, and homeostatic model assessment-estimated insulin resistance index; decreased serum insulin, leptin, hemoglobin A1c, and free fatty acids; and increased adiponectin. Shrimp oil also increased (p < 0.05) antioxidant capacity and reduced oxidative stress and chronic inflammation. The results demonstrated that shrimp oil dose-dependently improved glycemic control in obese rats through multiple mechanisms.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
C. Neves ◽  
T. Rodrigues ◽  
J. Sereno ◽  
C. Simões ◽  
J. Castelhano ◽  
...  

Nonalcoholic fatty liver disease (NAFLD) is caused by excessive liver lipid accumulation, but insulin resistance is specifically associated with impaired lipid saturation, oxidation, and storage (esterification), besides increased de novo lipogenesis. We hypothesized that dietary glycotoxins could impair hepatic lipid metabolism in obesity contributing to lipotoxicity-driven insulin resistance and thus to the onset of nonalcoholic steatohepatitis (NASH). In diet-induced obese rats with methylglyoxal-induced glycation, magnetic resonance spectroscopy, mass spectrometry, and gas chromatography were used to assess liver composition in fatty acyl chains and phospholipids. High-fat diet-induced obesity increased liver lipid fraction and suppressed de novo lipogenesis but did not change fatty acid esterification and saturation or insulin sensitivity. Despite a similar increase in total lipid fraction when supplementing the high-fat diet with dietary glycotoxins, impairment in the suppression of de novo lipogenesis and decreased fatty acid unsaturation and esterification were observed. Moreover, glycotoxins also decreased polyunsaturated cardiolipins and caused oxidative stress, portal inflammation, and insulin resistance in high-fat diet-induced obese rats. Dietary glycated products do not change total lipid levels in the liver of obese rats but dramatically modify the lipidemic profile, leading to oxidative stress, hepatic lipotoxicity, and insulin resistance in obesity and thus contribute to the onset of NASH.


Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1284-1289 ◽  
Author(s):  
Minghong Jiang ◽  
Yuhao Zhang ◽  
Meng Liu ◽  
Michael Shihli Lan ◽  
Jing Fei ◽  
...  

Abstract Obesity-dependent insulin resistance and type 2 diabetes mellitus are closely associated with decreased glucose utilization and down-regulation of hepatic glycolytic enzymes expression. Previously, we showed that DNA hypermethylation is involved in age-dependent susceptibility to hepatic insulin resistance and diabetes. However, what we cannot distinguish is whether the age-related obesity contributes to DNA hypermethylation in those natural aging rats. In the present study, we hypothesize that DNA methylation plays a crucial role in the regulation of glycolytic enzymes in the high-fat diet–induced obesity. Here, we report that DNA hypermethylation is correlated with a decline in hepatic glucokinase (Gck) and L-type pyruvate kinase (LPK) expression in high-fat diet–induced obese rats as compared with the control diet group. Down-regulation of Gck and LPK expression are reversed by the 5-aza-2′-deoxycytidine in the cell model of steatosis. These novel observations indicate that DNA methylation is involved in the development of metabolic diseases, such as obesity, insulin resistance, type 2 diabetes mellitus, and nonalcoholic steatohepatitis, suggesting that the hypermethylation level of Gck and LPK promoters may be a useful parameter for the evaluation of obesity-induced insulin resistance and fatty liver.


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