High fat diet causes rebound weight gain

Acknowledgements This work was funded by a grant from Action Medical Research (SP4581). We are grateful to the animal house staff for looking after the animals.Peer reviewedPublisher PD

Effects of Prebiotics, Probiotics, and Synbiotics on the Bodyweight, Blood Glucose, Triglyceride and TNF-α of Diet-induced Obesity Rats

Abstract  High-fat diet leads to obesity-associated chronic low-grade inflammation. Prebiotics, probiotics, and synbiotics produced short-chain fatty acids (SCFA), bonded to G protein-coupled receptors (GPR)-41 and GPR-43 decreased triglyceride deposits in adipocytes and liver, decreased fatty acid oxidation, increased glucose regulation and insulin sensitivity thus reduced the risk of obesity and metabolic syndrome. This study conducted in order to evaluate the effects of prebiotics, probiotics, and synbiotics on the body weight, blood glucose, triglyceride, and TNF-α used rats model, which were fed by a high-fat diet. Thirty-eight 6-8 weeks old male rats were fed by high-fat diet for three weeks, then rats were randomly divided into four groups, high-fat diet (HFD), a high fat diet with prebiotics supplementation (HFD+ PRE), a high fat diet with probiotics supplementation (HFD+PRO), and high-fat diet with synbiotics supplementation (HFD+SYN) for three weeks. Blood samples and body weight were measured at the third and sixth week. There was no effect of prebiotics, probiotics, and synbiotics on body weight, triglyceride levels, blood glucose, and TNF-α in rats fed a high-fat diet compared to control. These results suggested that supplementations gave inconsistent results with other studies and needed further researches.Keywords             : high fat diet, prebiotics, probiotics, synbiotics, meta-inflammationCorrespondence   : [email protected]

High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability.

The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in leptin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease

Phenotypic Changes in Diabetic Neuropathy Induced by a High-Fat Diet in Diabetic C57Bl/6 Mice

Emerging evidence suggests that dyslipidemia is an independent risk factor for diabetic neuropathy (DN) (reviewed by Vincent et al. 2009). To experimentally determine how dyslipidemia alters DN, we quantified neuropathic symptoms in diabetic mice fed a high-fat diet. Streptozotocin-induced diabetic C57BL/6 mice fed a high-fat diet developed dyslipidemia and a painful neuropathy (mechanical allodynia) instead of the insensate neuropathy (mechanical insensitivity) that normally develops in this strain. Nondiabetic mice fed a high-fat diet also developed dyslipidemia and mechanical allodynia. Thermal sensitivity was significantly reduced in diabetic compared to nondiabetic mice, but was not worsened by the high-fat diet. Moreover, diabetic mice fed a high-fat diet had significantly slower sensory and motor nerve conduction velocities compared to nondiabetic mice. Overall, dyslipidemia resulting from a high-fat diet may modify DN phenotypes and/or increase risk for developing DN. These results provide new insight as to how dyslipidemia may alter the development and phenotype of diabetic neuropathy

Wheel-running activity modulates circadian organization and the daily rhythm of eating behavior

Consumption of high-fat diet acutely alters the daily rhythm of eating behavior and circadian organization (the phase relationship between oscillators in central and peripheral tissues) in mice. Voluntary wheel-running activity counteracts the obesogenic effects of high-fat diet and also modulates circadian rhythms in mice. In this study, we sought to determine whether voluntary wheel-running activity could prevent the proximate effects of high-fat diet consumption on circadian organization and behavioral rhythms in mice. Mice were housed with locked or freely rotating running wheels and fed chow or high-fat diet for 1 week and rhythms of locomotor activity, eating behavior, and molecular timekeeping (PERIOD2::LUCIFERASE luminescence rhythms) in ex vivo tissues were measured. Wheel-running activity delayed the phase of the liver rhythm by 4 h in both chow- and high-fat diet-fed mice. The delayed liver phase was specific to wheel-running activity since an enriched environment without the running wheel did not alter the phase of the liver rhythm. In addition, wheel-running activity modulated the effect of high-fat diet consumption on the daily rhythm of eating behavior. While high-fat diet consumption caused eating events to be more evenly dispersed across the 24 h-day in both locked-wheel and wheel-running mice, the effect of high-fat diet was much less pronounced in wheel-running mice. Together these data demonstrate that wheel-running activity is a salient factor that modulates liver phase and eating behavior rhythms in both chow- and high-fat-diet fed mice. Wheel-running activity in mice is both a source of exercise and a self-motivating, rewarding behavior. Understanding the putative reward-related mechanisms whereby wheel-running activity alters circadian rhythms could have implications for human obesity since palatable food and exercise may modulate similar reward circuits

Addition of conjugated linoleic acid in whole milk improves lipid profile in high fat diet induced hypercholesterolemia of rats

Conjugated linoleic acid (CLA) is an isomer of linoleic acid that has been shown to havemany beneficial effects in prevention of atherosclerosis, hypertension, cardiovasculardiseases and improve immune function. Although majority of CLA in the diet are derivedfrom dairy product such as milk, however, the content of CLA in milk is affected by cow’sdiet. The aim of this study was to investigate the beneficial effect of CLA supplementationin milk for improving lipid profile in high fat diet of rats. Twenty four male Sprague Dawleyrats aged 8 weeks were given high fat diet for 3 weeks to induce hypercholesterolemia.Six rats were maintained in standard diet as control. Rats then were divided into 4 groupsi.e. normal control, negative control, high fat diet+CLA 0.5%, high fat diet + CLA 0.5%supplemented skim milk, and high fat diet + CLA 0.5% supplemented whole milk. Bloodsample was drawn after high fat diet induced hypercholesterolemia and after 4 weeksof treatment for total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDLcholesterol), and high density lipoprotein cholesterol (HDL cholesterol) analysis. Bodyweight was measured each week. Results showed that body weight was significantlyincrease in all groups received high fat diet (p0.05). Total cholesterol, triglyceride, andLDL cholesterol was significantly decrease in whole milk followed by significant increasein HDL cholesterol level. Skim milk supplemented with CLA had only modest effect ontriglyceride and HDL cholesterol level. In conclusion, CLA supplementation in whole milkimproves lipid profile in high fat diet

The Behavioral and Physiological Effects of High-fat Diet and Alcohol Consumption: Sex Differences in C57BL6/J Mice

Background and Objective: Animal studies can be a great tool to investigate sex differences in a variety of different ways, including behavioral and physiological responses to drug treatments and different “lifestyle variables” such as diets. Consumption of both high-fat diets and alcohol is known to affect anxiety behaviors and overall health. This project investigated how high-fat diet and alcohol access and its combination affected the behavior and physiology of male and female C57BL/6J mice. Method: Mice were separated into three food groups: high-fat diet, 10% fat diet, and regular chow, and each group was paired with either water or 10% alcohol. Behavioral assays included diet and alcohol preference, light-dark box, open field, and feeding and drinking measurements. Physiological measures included glucose tolerance tests and measurement of brain-derived neurotrophic factor, insulin, and leptin levels. Results: Females and males differed in the open field, as male mice decreased activity, while females increased activity when consuming high-fat diet. While females consumed more ethanol than males, alcohol consumption was able to improve glucose tolerance and increase anxiety in both sexes. Lastly, females were more resistant to the physiological changes caused by high-fat diet than males, as females consuming high-fat diet exhibited decreased insulin secretion, less change to brain-derived neurotrophic factor levels, and better glucose tolerance than males consuming high-fat diet. Conclusion: These results suggest that the response to high-fat diet and alcohol consumption is sex dependent and that males are more affected both behaviorally and physiologically by high-fat diet compared to females

Fecal Viral Community Responses to High-Fat Diet in Mice.

Alterations in diet can have significant impact on the host, with high-fat diet (HFD) leading to obesity, diabetes, and inflammation of the gut. Although membership and abundances in gut bacterial communities are strongly influenced by diet, substantially less is known about how viral communities respond to dietary changes. Examining fecal contents of mice as the mice were transitioned from normal chow to HFD, we found significant changes in the relative abundances and the diversity in the gut of bacteria and their viruses. Alpha diversity of the bacterial community was significantly diminished in response to the diet change but did not change significantly in the viral community. However, the diet shift significantly impacted the beta diversity in both the bacterial and viral communities. There was a significant shift away from the relatively abundant Siphoviridae accompanied by increases in bacteriophages from the Microviridae family. The proportion of identified bacteriophage structural genes significantly decreased after the transition to HFD, with a conserved loss of integrase genes in all four experimental groups. In total, this study provides evidence for substantial changes in the intestinal virome disproportionate to bacterial changes, and with alterations in putative viral lifestyles related to chromosomal integration as a result of shift to HFD.IMPORTANCE Prior studies have shown that high-fat diet (HFD) can have profound effects on the gastrointestinal (GI) tract microbiome and also demonstrate that bacteria in the GI tract can affect metabolism and lean/obese phenotypes. We investigated whether the composition of viral communities that also inhabit the GI tract are affected by shifts from normal to HFD. We found significant and reproducible shifts in the content of GI tract viromes after the transition to HFD. The differences observed in virome community membership and their associated gene content suggest that these altered viral communities are populated by viruses that are more virulent toward their host bacteria. Because HFD also are associated with significant shifts in GI tract bacterial communities, we believe that the shifts in the viral community may serve to drive the changes that occur in associated bacterial communities