Effects of high-fat diet-induced obesity and diabetes on Kiss1 and GPR54 expression in the hypothalamic–pituitary–gonadal (HPG) axis and peripheral organs (fat, pancreas and liver) in male rats

Neuropeptides ◽  
2016 ◽  
Vol 56 ◽  
pp. 41-49 ◽  
Author(s):  
M. Dudek ◽  
P.A. Kołodziejski ◽  
E. Pruszyńska-Oszmałek ◽  
M. Sassek ◽  
K. Ziarniak ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Hpg Axis ◽  
Peripheral Organs ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

scholarly journals High-Fat Diet and Age-Dependent Effects of IgA-Bearing Cell Populations in the Small Intestinal Lamina Propria in Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1165
Author(s):  
Yuta Sakamoto ◽  
Masatoshi Niwa ◽  
Ken Muramatsu ◽  
Satoshi Shimo
Keyword(s):  
Immune Function ◽  
Lamina Propria ◽  
High Fat Diet ◽  
Immunoglobulin A ◽  
Immune Functions ◽  
High Fat ◽  
Intestinal Villi ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Several studies highlighted that obesity and diabetes reduce immune function. However, changes in the distribution of immunoglobins (Igs), including immunoglobulin-A (IgA), that have an important function in mucosal immunity in the intestinal tract, are unclear. This study aimed to investigate the impaired immune functions in the context of a diet-induced obese murine model via the assessment of the Igs in the intestinal villi. We used mice fed a high-fat diet (HFD) from four to 12 or 20 weeks of age. The distributions of IgA, IgM, and IgG1 were observed by immunohistochemistry. Interestingly, we observed that IgA was immunolocalized in many cells of the lamina propria and that immunopositive cells increased in mice aged 12 to 20 weeks. Notably, mice fed HFD showed a reduced number of IgA-immunopositive cells in the intestinal villi compared to those fed standard chow. Of note, the levels of IgM and IgG1 were also reduced in HFD fed mice. These results provide insights into the impaired mucosal immune function arising from diet-induced obesity and type 2 diabetes.

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

2007 ◽  
Vol 293 (1) ◽  
pp. E31-E41 ◽  
Author(s):  
Robert C. Noland ◽  
John P. Thyfault ◽  
Sarah T. Henes ◽  
Brian R. Whitfield ◽  
Tracey L. Woodlief ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Gain ◽  
High Fat Diet ◽  
Oxidative Capacity ◽  
Male Rats ◽  
High Fat ◽  
Endurance Running ◽  
Muscle Oxidative Capacity ◽  
Obesity And Diabetes

Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.

scholarly journals Reversal of Diet-Induced Obesity Increases Insulin Transport into Cerebrospinal Fluid and Restores Sensitivity to the Anorexic Action of Central Insulin in Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (3) ◽  
pp. 1047-1054 ◽  
Author(s):  
Denovan P. Begg ◽  
Joram D. Mul ◽  
Min Liu ◽  
Brianne M. Reedy ◽  
David A. D'Alessio ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
High Fat Diet ◽  
Male Rats ◽  
Control Group ◽  
Chow Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Insulin Transport ◽  
The Central Nervous System

Abstract Diet-induced obesity (DIO) reduces the ability of centrally administered insulin to reduce feeding behavior and also reduces the transport of insulin from the periphery to the central nervous system (CNS). The current study was designed to determine whether reversal of high-fat DIO restores the anorexic efficacy of central insulin and whether this is accompanied by restoration of the compromised insulin transport. Adult male Long-Evans rats were initially maintained on either a low-fat chow diet (LFD) or a high-fat diet (HFD). After 22 weeks, half of the animals on the HFD were changed to the LFD, whereas the other half continued on the HFD for an additional 8 weeks, such that there were 3 groups: 1) a LFD control group (Con; n = 18), 2) a HFD-fed, DIO group (n = 17), and 3) a HFD to LFD, DIO-reversal group (DIO-rev; n = 18). The DIO reversal resulted in a significant reduction of body weight and epididymal fat weight relative to the DIO group. Acute central insulin administration (8 mU) reduced food intake and caused weight loss in Con and DIO-rev but not DIO rats. Fasting cerebrospinal fluid insulin was higher in DIO than Con animals. However, after a peripheral bolus injection of insulin, cerebrospinal fluid insulin increased in Con and DIO-rev rats but not in the DIO group. These data provide support for previous reports that DIO inhibits both the central effects of insulin and insulin's transport to the CNS. Importantly, DIO-rev restored sensitivity to the effects of central insulin on food intake and insulin transport into the CNS.

New Prebiotics to Ameliorate High-Fat Diet-Induced Obesity and Diabetes via Modulation of Microbiome-Gut-Brain Axis

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 264-LB ◽  
Author(s):  
SHOKOUH AHMADI ◽  
RAVINDER K. NAGPAL ◽  
SHAOHUA WANG ◽  
HARIOM YADAV
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Chronic administration of Norwegian Ascophyllum nodosum phytocomplex inhibits high-fat-diet-induced obesity in male rats

Nutrafoods ◽  
2014 ◽  
Vol 13 (3) ◽  
pp. 113-122
Author(s):  
Stefania Murzilli ◽  
Donata Di Tommaso ◽  
Vincenzo Di Matteo ◽  
Luisa Sciulli ◽  
Daniela Corna ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Chronic Administration ◽  
Ascophyllum Nodosum ◽  
Male Rats ◽  
High Fat ◽  
Diet Induced Obesity

Chronic high-fat diet increases acute neuroendocrine stress response independently of prenatal dexamethasone treatment in male rats

2013 ◽  
Vol 26 (1) ◽  
pp. 8-18 ◽  
Author(s):  
Anders Abildgaard ◽  
Sten Lund ◽  
Karin S Hougaard
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
High Fat Diet ◽  
Forced Swim Test ◽  
Male Rats ◽  
Adolescent Male ◽  
Late Adolescent ◽  
High Fat ◽  
Obesity And Diabetes ◽  
Increased Risk

ObjectiveIntrauterine growth restriction (IUGR) has been associated with metabolic disorders later in life such as obesity and diabetes as well as psychiatric disorders such as depression and schizophrenia. Therefore, we wanted to investigate whether behavioural, metabolic or neuroendocrine abnormalities could be provoked or exacerbated by a high-fat diet (HFD) in an experimental model of IUGR.MethodsPregnant dams were exposed to dexamethasone (DEX) in the third gestational week to induce IUGR. Late adolescent male offspring of DEX- and vehicle-treated dams were then fed a HFD or standard chow for 8 weeks and subjected to a variety of assessments.ResultsOnly diet affected the hypothalamus-pituitary-adrenal (HPA) axis stress response, as HFD doubled the observed corticosterone levels following acute restraint. HFD and prenatal DEX exposure concomitantly exacerbated depressive-like behaviour in the forced swim test, even though no interaction was seen. Prenatal DEX treatment tended to increase the basal acoustic startle response (ASR), while an interaction between HFD and DEX was present in the ASR pre-pulse inhibition suggestive of fundamental changes in neuronal gating mechanisms. Metabolic parameters were only affected by diet, as HFD increased fasting glucose and insulin levels.ConclusionWe conclude that chronic HFD may be more important in programming of the HPA axis stress responsiveness than an adverse foetal environment and therefore potentially implies an increased risk for developing psychiatric and metabolic disease.

scholarly journals OR-006 Effect of Moderate-intensity Exercise on the Expression of Hypothalamic KiSS-1 and GPR54 mRNA in Diet Induced Obesity Rats

2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Yi Yan ◽  
Chunyu Liang ◽  
Rui Xu
Keyword(s):  
High Fat Diet ◽  
Normal Diet ◽  
Treadmill Training ◽  
Male Rats ◽  
Moderate Intensity ◽  
High Fat ◽  
Moderate Intensity Exercise ◽  
Diet Induced Obesity ◽  
Sd Rats ◽  
Fat Feeding

Objective To observe the effect of high fat diet on the hypothalamic expression of KiSS-1and the G-protein coupled receptor (GPR) 54 mRNA and explore the modulatory role of moderate-intensity exercise in the diet induced obesity male rats. Methods After 8 weeks high fat feeding, 20 obesity 11-weeks SD rats were randomly assigned to high-fat diet sedentary (FS, n=8) and high-fat diet exercise (FE, n=8) groups, 20 normal diet 11-weeks SD rats also were randomly assigned to sedentary (SS, n=8) and exercise (SE, n=8) groups. During the following 8 weeks, obesity rats were continued expose to high-fat-diet. SE and FE groups did the 60%-70%V(•)O2max treadmill training (5 days/week, 1 hour/day). The V(•)O2 max of exercise groups were remeasured every two weeks. The hypothalamic expression of KiSS-1 and GPR54 mRNA were tested in each group. Results After the first 8-weeks high fat feeding, the obesity rats were heavier than normal diet group (491.74±26.19g vs. 410.05±45.77g, p<0.01). After 8-weeks training, the FE group was lighter than FS group (590.23±35.74g vs. 681±52.56, p<0.01). The FS group had higher hypothalamic expression of KiSS-1 mRNA (1.51±0.66 vs 0.75±0.27, p<0.05) and GPR54 mRNA (2.45±0.38 vs 0.61±0.15, p<0.01) than SS group. The FE group had lower hypothalamic expression of KiSS-1 mRNA (0.69±0.13, p>0.05) and GPR54 mRNA (0.58±0.10, p<0.01) than FS group. Conclusions There is stimulating effect of high-fat diet induced obesity on hypothalamic expression of KiSS-1and GPR54 mRNA. 8-weeks 60%-70%V (•) O2max treadmill training could cure this effect.  

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