scholarly journals Impaired adaptation of energy intake induces severe obesity in aged mice on a high-fat diet

2019 ◽  
Vol 7 (3) ◽  
pp. e13989
Author(s):  
Tadashi Okada ◽  
Yuichiro Mita ◽  
Hideyuki Sakoda ◽  
Masamitsu Nakazato
Keyword(s):  
Energy Intake ◽  
High Fat Diet ◽  
Severe Obesity ◽  
High Fat ◽  
Aged Mice

Mice with deletion of the mitochondrial glycerol-3-phosphate dehydrogenase gene exhibit a thrifty phenotype: effect of gender

2004 ◽  
Vol 287 (1) ◽  
pp. R147-R156 ◽  
Author(s):  
Assim Alfadda ◽  
Rosangela A. DosSantos ◽  
Zaruhi Stepanyan ◽  
Husnia Marrif ◽  
J. Enrique Silva
Keyword(s):  
Energy Intake ◽  
High Fat Diet ◽  
Female Gender ◽  
Intermediary Metabolism ◽  
High Fat ◽  
Serum Triglycerides ◽  
Female Mice ◽  
Thrifty Phenotype ◽  
Glycerol 3 Phosphate Dehydrogenase ◽  
Ad Libitum Intake

To define the role of mitochondrial glycerol-3-phosphate dehydrogenase (mGPD; EC 1.1.99.5 ) in energy balance and intermediary metabolism, we studied transgenic mice not expressing mGPD (mGPD−/−). These mice had ≈14% lower blood glucose; ≈50% higher serum glycerol; ≈80% higher serum triglycerides; and at thermoneutrality, their energy expenditure (Qo2) was 15% lower than in wild-type (WT) mice. Glycerol-3-phosphate levels and lactate-to-pyruvate ratios were threefold elevated in muscle, but not in liver, of mGPD−/− mice. WT and mGPD−/− mice were then challenged with a high-fat diet, fasting, or food restriction. The high-fat diet caused more weight gain and adiposity in mGPD−/− than in WT female mice, without the genotype differentially affecting Qo2 or energy intake. After a 30-h fast, WT female lost 60% more weight than mGPD−/− mice but these latter became more hypothermic. When energy intake was restricted to 50–70% of the ad libitum intake for 10 days, mGPD−/− female mice lost less weight than WT controls, but they had lower Qo2 and body temperature. WT and mGPD−/− male mice did not differ significantly in their responses to these challenges. These results show that the lack of mGPD causes significant alterations of intermediary metabolism, which are more pronounced in muscle than liver and lead to a thrifty phenotype that is more marked in females than males. Lower T4-to-T3 conversion in mGPD−/− females and a greater reliance of normal females on mGPD to respond to high-fat diets make the lack of the enzyme more consequential in the female gender.

Effects Of CLA/n-3 and Resistance Training on Muscle Quality in Middle-aged Mice During High-fat Diet

2014 ◽  
Vol 46 ◽  
pp. 588
Author(s):  
Seung-Lyul Oh ◽  
Sang-Rok Lee ◽  
Andy V. Khamoui ◽  
Edward Jo ◽  
Bong-Sup Park ◽  
...  
Keyword(s):  
Resistance Training ◽  
High Fat Diet ◽  
Muscle Quality ◽  
High Fat ◽  
Middle Aged ◽  
Aged Mice

scholarly journals Decrease of Obesity by Allantoin via Imidazoline I1-Receptor Activation in High Fat Diet-Fed Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Hsien-Hui Chung ◽  
Kung Shing Lee ◽  
Juei-Tang Cheng
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Intake ◽  
High Fat Diet ◽  
Chronic Administration ◽  
Receptor Activation ◽  
Inhibitory Effect ◽  
High Fat ◽  
Epididymal White Adipose Tissue ◽  
The Brain

The activation of the imidazoline I1-receptor (I1R) is known to regulate appetite. Allantoin, an active ingredient in the yam, has been reported to improve lipid metabolism in high fat diet- (HFD-)fed mice. However, the effect of allantoin on obesity remains unclear. In the present study, we investigated the effects of allantoin on HFD-induced obesity. The chronic administration of allantoin to HFD-fed mice for 8 weeks significantly decreased their body weight, and this effect was reversed by efaroxan at a dose sufficient to block I1R. The epididymal white adipose tissue (eWAT) cell size and weight in HFD-fed mice were also decreased by allantoin via the activation of I1R. In addition, allantoin significantly decreased the energy intake of HFD-fed mice, and this reduction was associated with a decrease in the NPY levels in the brain. However, no inhibitory effect of allantoin on energy intake was observed in db/db mice. Moreover, allantoin lowered HFD-induced hyperleptinemia, and this activity was abolished by I1R blockade with efaroxan. Taken together, these data suggest that allantoin can ameliorate energy intake and eWAT accumulation by activating I1R to improve HFD-induced obesity.

scholarly journals Dietary α-lactalbumin alters energy balance, gut microbiota composition and intestinal nutrient transporter expression in high-fat diet-fed mice

2019 ◽  
Vol 121 (10) ◽  
pp. 1097-1107 ◽  
Author(s):  
Serena Boscaini ◽  
Raul Cabrera-Rubio ◽  
John R. Speakman ◽  
Paul D. Cotter ◽  
John F. Cryan ◽  
...  
Keyword(s):  
Energy Balance ◽  
Gut Microbiota ◽  
Whey Protein ◽  
Energy Intake ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Whey Proteins ◽  
Nutrient Transporters ◽  
High Fat ◽  
Cumulative Energy

AbstractRecently there has been a considerable rise in the frequency of metabolic diseases, such as obesity, due to changes in lifestyle and resultant imbalances between energy intake and expenditure. Whey proteins are considered as potentially important components of a dietary solution to the obesity problem. However, the roles of individual whey proteins in energy balance remain poorly understood. This study investigated the effects of a high-fat diet (HFD) containing α-lactalbumin (LAB), a specific whey protein, or the non-whey protein casein (CAS), on energy balance, nutrient transporters expression and enteric microbial populations. C57BL/6J mice (n 8) were given an HFD containing either 20 % CAS or LAB as protein sources or a low-fat diet containing CAS for 10 weeks. HFD-LAB-fed mice showed a significant increase in cumulative energy intake (P=0·043), without differences in body weight, energy expenditure, locomotor activity, RER or subcutaneous and epididymal white adipose tissue weight. HFD-LAB intake led to a decrease in the expression of glut2 in the ileum (P=0·05) and in the fatty acid transporter cd36 (P<0·001) in both ileum and jejunum. This suggests a reduction in absorption efficiency within the small intestine in the HFD-LAB group. DNA from faecal samples was used for 16S rRNA-based assessment of intestinal microbiota populations; the genera Lactobacillus, Parabacteroides and Bifidobacterium were present in significantly higher proportions in the HFD-LAB group. These data indicate a possible functional relationship between gut microbiota, intestinal nutrient transporters and energy balance, with no impact on weight gain.

scholarly journals Modifications of gastric inhibitory polypeptide (GIP) secretion in man by a high-fat diet

1988 ◽  
Vol 59 (3) ◽  
pp. 373-380 ◽  
Author(s):  
L. M. Morgan ◽  
S. M. Hampton ◽  
J. A. Tredger ◽  
R. Cramb ◽  
V. Marks
Keyword(s):  
Glucose Tolerance ◽  
Energy Intake ◽  
Plasma Glucose ◽  
High Fat Diet ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose ◽  
Fat Intake ◽  
High Fat ◽  
C Peptide ◽  
Glucose Levels

1. Five healthy volunteers (usual fat intake 103) (SE 9) g/d and energy intake 9855 (SE 937) kJ/d were given on two separate occasions (a) 100 g oral glucose and (b) sufficient intravenous (IV) glucose to obtain similar arterialized plasma glucose levels to those after oral glucose.2. Subjects increased their fat intake by 68 (SE 9·6) % for 28 d by supplementing their diet with 146 ml double cream/d (fat intake on high-fat diet (HFD) 170 (SE 8) g/d; energy intake 12347 (SE 770)).3. The 100 g oral glucose load was repeated and IV glucose again given in quantities sufficient to obtain similar arterialized blood glucose levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide (GIP) were measured.4. Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0–180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P < 0·05). Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P < 0·01) but neither were affected by the HFD. Glucose levels were lower following the HFD after both oral and IV glucose (area under plasma glucose curve 0–180 min, following oral glucose 6·7 (SE 0·3) mmol/l.h for control and 4·2 (SE 0·6) mmol/l.h for HFD; P < 0·01).5. Glucose-stimulated GIP secretion was thus enhanced by the HFD. Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance.6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine.

scholarly journals Spatial Cognition in Adult and Aged Mice Exposed to High-Fat Diet

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0140034 ◽  
Author(s):  
James P. Kesby ◽  
Jane J. Kim ◽  
Miriam Scadeng ◽  
Gina Woods ◽  
Deborah M. Kado ◽  
...  
Keyword(s):  
Spatial Cognition ◽  
High Fat Diet ◽  
High Fat ◽  
Aged Mice

scholarly journals Kappa-Carrageenan Inhibited the High-Fat-Diet-Induced Obesity Through Up-Regulating the Hepatic Sirt1 Gene Expression

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 503-503
Author(s):  
Zhiji Huang ◽  
Yafang Ma ◽  
Chunbao Li
Keyword(s):  
Gene Expression ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Energy Intake ◽  
High Fat Diet ◽  
The Body ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Sirt1 Gene ◽  
Kappa Carrageenan

Abstract Objectives Kappa-Carrageenan(CGN) is a widely used food additive in the meat industry and a highly viscous soluble dietary fiber which can hardly be fermented. It has been shown to be able to regulate the energy metabolism and inhibit diet-induced obesity. However, the mechanism is not well understood. The purpose of this study is to investigate the mechanisms of κ-carrageenan to inhibit the body weight gain. Methods A high-fat diet incorporated with lard, pork protein and CGN (2% or 4%, w/w) was given to C57BL/6J mice for 90 days. The energy intake and weight changes were measured every three days. After the dietary intervention, mice were sacrificed, liver and epididymal adipose tissues were taken for real-time polymerase chain reaction (RT-qPCR) analysis. Results The CGN in the high-fat diet restricted weight gain by decreasing liver and adipose mass without inhibiting energy intake.  The genes involving energy expenditure such as Acox1, Acadl, CPT-1A and Sirt1 were upregulated in the mice fed with carrageenan. However, the genes responsible for lipid synthesis were not significantly different compared to the diet-induced obese model. Conclusions The anti-obesity effect of the CGN in high-fat diet could be highly related to the enhancement of energy expenditure through up-regulating the downstream genes which promote β-oxidation by increasing the Sirt1 gene expression in liver. Funding Sources Ministry of Science and Technology of the People's Republic of China (10000 Talent Project)

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