scholarly journals Glucose-dependent insulinotropic polypeptide is required for moderate high-fat diet- but not high-carbohydrate diet-induced weight gain

2018 ◽  
Vol 314 (6) ◽  
pp. E572-E583 ◽  
Author(s):  
Ryuya Maekawa ◽  
Hidetada Ogata ◽  
Masatoshi Murase ◽  
Norio Harada ◽  
Kazuyo Suzuki ◽  
...  

Both high-fat (HFD) and high-carbohydrate (ST) diets are known to induce weight gain. Glucose-dependent insulinotropic polypeptide (GIP) is secreted mainly from intestinal K cells upon stimuli by nutrients such as fat and glucose, and it potentiates glucose-induced insulin secretion. GIP is well known to contribute to HFD-induced obesity. In this study, we analyzed the effect of ST feeding on GIP secretion and metabolic parameters to explore the role of GIP in ST-induced weight gain. Both wild-type (WT) and GIP receptor deficient ( GiprKO) mice were fed normal chow (NC), ST, or moderate (m)HFD for 22 wk. Body weight was measured, and then glucose tolerance tests were performed. Insulin secretion from isolated islets also was analyzed. WT mice fed ST or mHFD displayed weight gain concomitant with increased plasma GIP levels compared with WT mice fed NC. WT mice fed mHFD showed improved glucose tolerance due to enhanced insulin secretion during oral glucose tolerance tests compared with WT mice fed NC or ST. GiprKO mice fed mHFD did not display weight gain. On the other hand, GiprKO mice fed ST showed weight gain and did not display obvious glucose intolerance. Glucose-induced insulin secretion was enhanced during intraperitoneal glucose tolerance tests and from isolated islets in both WT and GiprKO mice fed ST compared with those fed NC. In conclusion, enhanced GIP secretion induced by mHFD-feeding contributes to increased insulin secretion and body weight gain, whereas GIP is marginally involved in weight gain induced by ST-feeding.

2010 ◽  
Vol 61 (4) ◽  
pp. 355-363 ◽  
Author(s):  
Zsuzsa Iffiú-Soltész ◽  
Estelle Wanecq ◽  
Almudena Lomba ◽  
Maria P. Portillo ◽  
Federica Pellati ◽  
...  

Endocrinology ◽  
2015 ◽  
Vol 156 (11) ◽  
pp. 4047-4058 ◽  
Author(s):  
Yun-Jung Lee ◽  
Conglin Liu ◽  
Mengyang Liao ◽  
Galina K. Sukhova ◽  
Jun Shirakawa ◽  
...  

Prior studies demonstrated increased plasma IgE in diabetic patients, but the direct participation of IgE in diabetes or obesity remains unknown. This study found that plasma IgE levels correlated inversely with body weight, body mass index, and body fat mass among a population of randomly selected obese women. IgE receptor FcϵR1-deficient (Fcer1a−/−) mice and diet-induced obesity (DIO) mice demonstrated that FcϵR1 deficiency in DIO mice increased food intake, reduced energy expenditure, and increased body weight gain but improved glucose tolerance and glucose-induced insulin secretion. White adipose tissue from Fcer1a−/− mice showed an increased expression of phospho-AKT, CCAAT/enhancer binding protein-α, peroxisome proliferator-activated receptor-γ, glucose transporter-4 (Glut4), and B-cell lymphoma 2 (Bcl2) but reduced uncoupling protein 1 (UCP1) and phosphorylated c-Jun N-terminal kinase (JNK) expression, tissue macrophage accumulation, and apoptosis, suggesting that IgE reduces adipogenesis and glucose uptake but induces energy expenditure, adipocyte apoptosis, and white adipose tissue inflammation. In 3T3-L1 cells, IgE inhibited the expression of CCAAT/enhancer binding protein-α and peroxisome proliferator-activated receptor-γ, and preadipocyte adipogenesis and induced adipocyte apoptosis. IgE reduced the 3T3-L1 cell expression of Glut4, phospho-AKT, and glucose uptake, which concurred with improved glucose tolerance in Fcer1a−/− mice. This study established two novel pathways of IgE in reducing body weight gain in DIO mice by suppressing adipogenesis and inducing adipocyte apoptosis while worsening glucose tolerance by reducing Glut4 expression, glucose uptake, and insulin secretion.


Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2446
Author(s):  
Rebecca O’Rielly ◽  
Hui Li ◽  
See Meng Lim ◽  
Roger Yazbeck ◽  
Stamatiki Kritas ◽  
...  

Chronic isoleucine supplementation prevents diet-induced weight gain in rodents. Acute-isoleucine administration improves glucose tolerance in rodents and reduces postprandial glucose levels in humans. However, the effect of chronic-isoleucine supplementation on body weight and glucose tolerance in obesity is unknown. This study aimed to investigate the impact of chronic isoleucine on body weight gain and glucose tolerance in lean and high-fat-diet (HFD) induced-obese mice. Male C57BL/6-mice, fed a standard-laboratory-diet (SLD) or HFD for 12 weeks, were randomly allocated to: (1) Control: Drinking water; (2) Acute: Drinking water with a gavage of isoleucine (300 mg/kg) prior to the oral-glucose-tolerance-test (OGTT) or gastric-emptying-breath-test (GEBT); (3) Chronic: Drinking water with 1.5% isoleucine, for a further six weeks. At 16 weeks, an OGTT and GEBT was performed and at 17 weeks metabolic monitoring. In SLD- and HFD-mice, there was no difference in body weight, fat mass, and plasma lipid profiles between isoleucine treatment groups. Acute-isoleucine did not improve glucose tolerance in SLD- or HFD-mice. Chronic-isoleucine impaired glucose tolerance in SLD-mice. There was no difference in gastric emptying between any groups. Chronic-isoleucine did not alter energy intake, energy expenditure, or respiratory quotient in SLD- or HFD-mice. In conclusion, chronic isoleucine supplementation may not be an effective treatment for obesity or glucose intolerance.


2020 ◽  
Vol 150 (8) ◽  
pp. 2101-2111 ◽  
Author(s):  
Lili Tian ◽  
Hongmei Ning ◽  
Weijuan Shao ◽  
Zhuolun Song ◽  
Yasaman Badakhshi ◽  
...  

ABSTRACT Background Dietary polyphenols including anthocyanins target multiple organs. Objective We aimed to assess the involvement of glucagon-like peptide 1 (GLP-1), leptin, insulin and fibroblast growth factor 21 (FGF21) in mediating metabolic beneficial effects of purified anthocyanin cyanidin-3-glucoside (Cy3G). Methods Intestinal proglucagon gene (Gcg; encoding GLP-1) and liver Fgf21 expression were assessed in 6-wk-old male C57BL-6J mice fed a low-fat-diet (LFD; 10% of energy from fat), alone or with 1.6 mg Cy3G/L in drinking water for 3 wk [experiment (Exp.) 1; n = 5/group]. Similar mice were fed the LFD or a high-fat diet (HFD; 60% energy from fat) with or without Cy3G for 20 wk. Half of the mice administered Cy3G also received 4 broad-spectrum antibiotics (ABs) in drinking water between weeks 11 and 14, for a total of 6 groups (n = 8/group). Metabolic tolerance tests were conducted between weeks 2 and 16. Relevant hormone gene expression and plasma hormone concentrations were assessed mainly at the end of 20 wk (Exp. 2). Results In Exp. 1, Cy3G administration increased ileal but not colonic Gcg level by 2-fold (P < 0.05). In Exp. 2, Cy3G attenuated HFD-induced body-weight gain (20.3% at week 16), and improved glucose tolerance (26.5% at week 15) but not insulin tolerance. Although Cy3G had no effect on glucose tolerance in LFD mice, LFD/Cy3G/AB mice showed better glucose tolerance than LFD/Cy3G mice (23%). In contrast, HFD/Cy3G/AB mice showed worse glucose tolerance compared with HFD/Cy3G mice (15%). Beneficial effects of Cy3G in HFD mice were not associated with changes in plasma leptin, insulin or GLP-1 concentrations. However, Cy3G increased hepatic Fgf21 expression in mice in Exp. 1 by 4-fold and attenuated Fgf21 overexpression in HFD mice (Exp. 2, 22%), associated with increased expression of genes that encode FGFR1 and β-klotho (>3-fold, P < 0.05). Conclusions Dietary Cy3G may reduce body weight and exert metabolic homeostatic effects in mice via changes in hepatic FGF21.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 669-669
Author(s):  
Armando Tovar ◽  
Monica Sanchez-Tapia ◽  
Daniela Moreno ◽  
Guillermo Ordaz ◽  
Martha Guevara ◽  
...  

Abstract Objectives Several studies have demonstrated that the consumption of soy protein decreases LDL-cholesterol, improves insulin sensitivity and attenuates body weight gain. Also, soy protein consumption can modify the gut microbiota, however it has not been established whether the changes in gut microbiota are in part responsible of the health effects of soy protein. Thus, the aim of the present study was to understand whether the metabolic effects of soy protein are reduced by the use of an antibiotic treatment. Methods Rats were fed for 16 weeks with one of the 4 experimental diets: 1) Casein control diet (C), 2) Soy protein diet (S), 3) C high-fat diet, and 4) S high-fat diet. Each group was sub-divided at the end of the 16 weeks in 2 groups. One subgroup continue with the same diet, and the other received the antibiotic treatment (Ampicillin/Neomycin) for 4 weeks. During the study body weight, food intake, body composition, energy expenditure and glucose tolerance were measured. Fecal samples were collected before and after the antibiotic treatment to determine the gut microbiota using the Illumina platform. At the end of the study blood samples were obtained to measure several biochemical variables. Also, liver and adipose tissue samples were obtained to assess the abundance of mRNA and proteins involved in lipid, glucose and thermogenesis. Results Rats fed S or S high fat diet had significant lower body weight gain, body fat, energy expenditure, glucose tolerance, blood lipids, increased expression of thermogenic genes and decreased serum lipopolisacharide than the control or high fat groups fed C diets. The antibiotic treatment abolished the health benefits observed in rats fed the S diets, particularly energy expenditure and weight gain. These changes were associated with changes in the gut microbiota, since S consumption increased the abundance of the Akkermansia and Bifidobacterium genus. This effect on the gut microbiota was prevented by the antibiotic treatment and rats developed metabolic endotoxemia. Finally, the antibiotic treatment reduced the expression of thermogenic genes, particularly in rats fed S high fat diet. Conclusions This study indicates that the beneficial effects of soy protein consumption on health are significantly dependent on the gut microbiota. Funding Sources CONACYT, INCMNSZ.


2010 ◽  
Vol 15 (4) ◽  
pp. 262-266 ◽  
Author(s):  
Won-Hee Choi ◽  
Ji-Yun Ahn ◽  
Sun-A Kim ◽  
Tae-Wan Kim ◽  
Tae-Youl Ha

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33858 ◽  
Author(s):  
Amandine Everard ◽  
Lucie Geurts ◽  
Marie Van Roye ◽  
Nathalie M. Delzenne ◽  
Patrice D. Cani

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