Effects of Previous Feeding of a High Carbohydrate or a High Fat Diet on Changes in Body Weight and Body Composition of Fasted Rats

1975 ◽  
Vol 105 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Hiroo Suzuki ◽  
Hisako Goshi ◽  
Hiroshi Sugisawa
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
High Fat Diet ◽  
High Fat ◽  
High Carbohydrate ◽  
Fasted Rats

scholarly journals Adult offspring of high-fat diet-fed dams can have normal glucose tolerance and body composition

2014 ◽  
Vol 5 (3) ◽  
pp. 229-239 ◽  
Author(s):  
K. M. Platt ◽  
R. J. Charnigo ◽  
K. J. Pearson
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
High Fat ◽  
High Fat Diets ◽  
Normal Glucose ◽  
Fat Diets

Maternal high-fat diet consumption and obesity have been shown to program long-term obesity and lead to impaired glucose tolerance in offspring. Many rodent studies, however, use non-purified, cereal-based diets as the control for purified high-fat diets. In this study, primiparous ICR mice were fed purified control diet (10–11 kcal% from fat of lard or butter origin) and lard (45 or 60 kcal% fat) or butter (32 or 60 kcal% fat)-based high-fat diets for 4 weeks before mating, throughout pregnancy, and for 2 weeks of nursing. Before mating, female mice fed the 32 and 60% butter-based high-fat diets exhibited impaired glucose tolerance but those females fed the lard-based diets showed normal glucose disposal following a glucose challenge. High-fat diet consumption by female mice of all groups decreased lean to fat mass ratios during the 4th week of diet treatment compared with those mice consuming the 10–11% fat diets. All females were bred to male mice and pregnancy and offspring outcomes were monitored. The body weight of pups born to 45% lard-fed dams was significantly increased before weaning, but only female offspring born to 32% butter-fed dams exhibited long-term body weight increases. Offspring glucose tolerance and body composition were measured for at least 1 year. Minimal, if any, differences were observed in the offspring parameters. These results suggest that many variables should be considered when designing future high-fat diet feeding and maternal obesity studies in mice.

scholarly journals The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery

2019 ◽  
Author(s):  
Brandon Boland ◽  
Michael B. Mumphrey ◽  
Zheng Hao ◽  
Benji Gill ◽  
R. Leigh Townsend ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Body Composition ◽  
Body Weight ◽  
High Fat Diet ◽  
Body Weight Loss ◽  
Liver Weight ◽  
Receptor Subtypes ◽  
High Fat ◽  
Knockout Mouse Model ◽  
Gut Hormone

Background/Goals: The gut hormone PYY secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight. Methods: Here we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype mice made obese on high-fat diet. Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, HOMA-IR, and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice. Conclusions: PYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as GLP-1 remain to be investigated.

scholarly journals The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 585 ◽  
Author(s):  
Brandon Boland ◽  
Michael Mumphrey ◽  
Zheng Hao ◽  
Benji Gill ◽  
R. Townsend ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Body Composition ◽  
Body Weight ◽  
High Fat Diet ◽  
Peptide Yy ◽  
Body Weight Loss ◽  
Receptor Subtypes ◽  
High Fat ◽  
Knockout Mouse Model ◽  
Gut Hormone

Background/Goals: The gut hormone peptide YY (PYY) secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight. Methods: Here we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype (WT) mice made obese on high-fat diet. Results: Both male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, insulin resistance (HOMA-IR), and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice. Conclusions: PYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as glucagon-like peptide-1 (GLP-1) remain to be investigated.

scholarly journals Variations in body weight, food intake and body composition after long-term high-fat diet feeding in C57BL/6J mice

Obesity ◽  
2014 ◽  
Vol 22 (10) ◽  
pp. 2147-2155 ◽  
Author(s):  
Yongbin Yang ◽  
Daniel L. Smith ◽  
Karen D. Keating ◽  
David B. Allison ◽  
Tim R. Nagy
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Food Intake ◽  
High Fat Diet ◽  
High Fat

scholarly journals Long-Term Supplementation With Fruits and Vegetables Curbs High-Fat Diet/Obesity-Induced Changes in Body Composition and Favorably Affects Blood T Cell Phenotype in Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1126-1126
Author(s):  
Weimin Guo ◽  
Dayong Wu ◽  
Lijun Li ◽  
Edwin Ortega ◽  
Yankun Liu ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Weight Gain ◽  
T Cell ◽  
Fat Mass ◽  
High Fat Diet ◽  
Cd4 Cells ◽  
High Fat ◽  
Cell Profile

Abstract Objectives Obesity is associated with impaired immune function. However, impact of obesity on blood T cell profile is not well studied. The objectives of this study were to investigate the effects of high fat diet (HFD)-induced obesity and long-term fruits and vegetable (FV) consumption on body composition and blood T cell profile. Methods This is partial report from an ongoing study. A total of 240 male C57BL/6J mice were randomly assigned to 4 groups: low fat control (LF-C) or high-fat control (HF-C) diet alone, or together with 15% of a unique mixture of FV (w/w, equivalent to 7–9 servings F&V/d for human) (LF-FV or HF-FV). The feeding will continue until 50% mortality is reached in one group. Body weight, body composition (using MRI), and blood T cell profile (using FACS) are monitored longitudinally at different time points. The results reported here are those assessed when mice were 7 months old. Results After 7 months of feeding, mice fed HF-C gained more weight compared to those fed LF-C. Mice fed HF-FV or LF-FV diets had significantly reduced weight gain and fat mass, and higher muscle mass compared to those fed HF-C or LF-C diet, respectively. Mice fed HF-C also had significantly lower percentage of blood CD3+, CD4+, and CD8 + T cells compared with the LF-C. FV supplementation prevented HFD-induced decrease in percentage of CD3+ and CD4+ cells. Furthermore, both % CD3+ and CD4+ cells were negatively correlated with body weight (P < 0.001) or percentage of fat mass (P < 0.001), and positively associated with percentage of lean mass (P < 0.001). Conclusions Our results suggest that consuming large amounts of a unique mixture of F&V curbs HFD-induced body weight gain, reduces fat mass, and favorably affects blood T cell population. Ongoing studies will assess these analytes when mice are 16 months old, and again when one group reaches 50% mortality, and determine their correlations with functional measures of T cell response, host resistance to infection, health span, and mortality. Funding Sources This study was supported by the U.S. Department of Agriculture – Agricultural Research Service (ARS), under Agreement No. 58–1950-4–004.

scholarly journals A minor role for lipocalin 2 in high-fat diet-induced glucose intolerance

2011 ◽  
Vol 301 (5) ◽  
pp. E825-E835 ◽  
Author(s):  
Lucy S. Jun ◽  
C. Parker Siddall ◽  
Evan D. Rosen
Keyword(s):  
Insulin Resistance ◽  
Body Composition ◽  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Metabolic Phenotype ◽  
Chow Diet ◽  
High Fat

Adipose tissue controls energy homeostasis and systemic insulin sensitivity through the elaboration of a series of cytokines and hormones, collectively termed “adipokines.” We and others have identified Lcn2 as a novel adipokine, but its exact role in obesity-induced insulin resistance remains controversial. The aim of this study was to examine the metabolic phenotype of Lcn2−/− mice to clarify the role of Lcn2 in metabolism. Male and female Lcn2−/− and wild-type (WT) littermates were placed on either chow or high-fat diet (HFD) to characterize their metabolic phenotype. Studies included body weight and body composition, glucose and insulin tolerance tests, and adipokine expression studies in serum and in white adipose tissue (WAT). Neither chow nor HFD cohorts showed any differences in body weight or body composition. Chow-fed Lcn2−/− mice did not exhibit any difference in glucose homeostasis compared with WT mice. Fasting serum glucose levels were lower in the chow-fed Lcn2−/− mice, but this finding was not seen in the HFD cohort. Serum adiponectin, leptin, resistin, and RBP4 levels were not different between WT and Lcn2−/− on chow diet. HFD-fed male Lcn2−/− mice did display a small improvement in glucose tolerance, but no difference in insulin sensitivity was seen in either male or female Lcn2−/− mice on HFD. We conclude that the global ablation of Lcn2 has a minimal effect on obesity-associated glucose intolerance but does not appear to affect either age- or obesity-mediated insulin resistance in vivo.

scholarly journals High fat-fed GPR55 null mice display impaired glucose tolerance without concomitant changes in energy balance or insulin sensitivity but are less responsive to the effects of the cannabinoids rimonabant or Δ(9)-tetrahydrocannabivarin on weight gain

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9811
Author(s):  
Edward T. Wargent ◽  
Malgorzata Kepczynska ◽  
Mohamed Sghaier Zaibi ◽  
David C. Hislop ◽  
Jonathan R.S. Arch ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Wild Type ◽  
High Fat ◽  
Insulin Tolerance

Background The insulin-sensitizing phytocannabinoid, Δ(9)-tetrahydrocannabivarin (THCV) can signal partly via G-protein coupled receptor-55 (GPR55 behaving as either an agonist or an antagonist depending on the assay). The cannabinoid receptor type 1 (CB1R) inverse agonist rimonabant is also a GPR55 agonist under some conditions. Previous studies have shown varied effects of deletion of GPR55 on energy balance and glucose homeostasis in mice. The contribution of signalling via GPR55 to the metabolic effects of THCV and rimonabant has been little studied. Methods In a preliminary experiment, energy balance and glucose homeostasis were studied in GPR55 knockout and wild-type mice fed on both standard chow (to 20 weeks of age) and high fat diets (from 6 to 15 weeks of age). In the main experiment, all mice were fed on the high fat diet (from 6 to 14 weeks of age). In addition to replicating the preliminary experiment, the effects of once daily administration of THCV (15 mg kg−1 po) and rimonabant (10 mg kg−1 po) were compared in the two genotypes. Results There was no effect of genotype on absolute body weight or weight gain, body composition measured by either dual-energy X-ray absorptiometry or Nuclear Magnetic Resonance (NMR), fat pad weights, food intake, energy expenditure, locomotor activity, glucose tolerance or insulin tolerance in mice fed on chow. When the mice were fed a high fat diet, there was again no effect of genotype on these various aspects of energy balance. However, in both experiments, glucose tolerance was worse in the knockout than the wild-type mice. Genotype did not affect insulin tolerance in either experiment. Weight loss in rimonabant- and THCV-treated mice was lower in knockout than in wild-type mice, but surprisingly there was no detectable effect of genotype on the effects of the drugs on any aspect of glucose homeostasis after taking into account the effect of genotype in vehicle-treated mice. Conclusions Our two experiments differ from those reported by others in finding impaired glucose tolerance in GPR55 knockout mice in the absence of any effect on body weight, body composition, locomotor activity or energy expenditure. Nor could we detect any effect of genotype on insulin tolerance, so the possibility that GPR55 regulates glucose-stimulated insulin secretion merits further investigation. By contrast with the genotype effect in untreated mice, we found that THCV and rimonabant reduced weight gain, and this effect was in part mediated by GPR55.

scholarly journals The influence of novel GPR119 agonist on body weight, food intake and glucose metabolism in obesity rats provoked high-fat and -carbohydrate diet

2016 ◽  
Vol 62 (1) ◽  
pp. 44-49 ◽  
Author(s):  
Ivan Nikolaevich Tiurenkov ◽  
Denis Vladimirovich Kurkin ◽  
Dmitry Aleksandrovich Bakulin ◽  
Elena Vladimirovna Volotova ◽  
Mikhail Ayratovich Chafeev
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Food Intake ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Glucose Levels ◽  
High Carbohydrate ◽  
Blood Glucose Levels ◽  
Gpr119 Agonist

The search for new drugs for the treatment of type 2 diabetes mellitus (T2DM) and obesity remains an urgent problem. Drugs with influence on incretin system are widely used in the treatment of T2DM and obesity, since in addition to the hypoglycemic action of their inherent hypophagic effects. With the discovery of GPR119 receptor, there is the opportunity to pharmacological stimulation of endogenous secretion of incretins. Compound ZB-16 is active GPR119 agonist with IC50=7 nM. Its activation leads to increased secretion of the major incretins (GLP-1 and GIP), which are able to influence glucose metabolism and feeding behavior.Aims — to study the effect of GPR 119 receptor agonist compounds ZB-16 on blood glucose, body weight and food intake in rats with obesity.Material and methods.Male rats with initial weight 390—400 g were fed with high-carbohydrate and high-fat diet. During the next four weeks the animals orally received ZB-16 (1 mg/kg) and metformin (400 mg/kg) and then we assessed the level of water and food consumption, blood glucose levels, and performed oral glucose tolerance test (OGTT).Results.Compound ZB-16 and metformin reduced fasting blood glucose levels and weight of experimental animals, while the control rats gained weight. GPR119 agonist is more pronounced than metformin reduced the area under the curve «glucose of concentration—time» during the OGTT.Conclusions.Novel GPR119 agonist — ZB-16 is comparable to metformin in hypoglycemic and anorexigenic effect in animals with obesity caused high-carbohydrate and high-fat diet.

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