scholarly journals Hypothalamic PDE3B deficiency alters body weight and glucose homeostasis in mouse

2018 ◽  
Vol 239 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Maitrayee Sahu ◽  
Prashanth Anamthathmakula ◽  
Abhiram Sahu
Keyword(s):  
Body Weight ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Specific Response ◽  
Mrna Levels ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Phosphodiesterase 3B

Pharmacological studies have suggested hypothalamic phosphodiesterase-3B to mediate leptin and insulin action in regulation of energy homeostasis. Whereas Pde3b-null mice show altered energy homeostasis, it is unknown whether this is due to ablation of Pde3b in the hypothalamus. Thus, to address the functional significance of hypothalamic phosphodiesterase-3B, we used Pde3b flox/flox and Nkx2.1-Cre mice to generate Pde3b Nkx2.1KD mice that showed 50% reduction of phosphodiesterase-3B in the hypothalamus. To determine the effect of partial ablation of phosphodiesterase-3B in the hypothalamus on energy and glucose homeostasis, males and females were subjected to either a low- or high-fat diet for 19–21 weeks. Only female but not male Pde3b Nkx2.1KD mice on the low-fat diet showed increased body weight from 13 weeks onward with increased food intake, decreased fat pad weights and hypoleptinemia. Glucose tolerance was improved in high-fat diet-fed male Pde3b Nkx2.1KD mice in association with decreased phosphoenolpyruvate carboxykinase-1 and glucose-6-phosphatase mRNA levels in the liver. Also, insulin sensitivity was increased in male Pde3b Nkx2.1KD mice on the low-fat diet. Changes in body weight or in glucose homeostasis were not associated with any alteration in hypothalamic proopiomelanocortin, neuropepide Y and agouti-related peptide mRNA levels. These results suggest that partial loss of phosphodiesterase-3B in the hypothalamus produces a sex-specific response in body weight and glucose homeostasis, and support a role, at least in part, for hypothalamic phosphodiesterase-3B in regulation of energy and glucose homeostasis in mice.

scholarly journals Inactivation of the adrenergic receptor β2 disrupts glucose homeostasis in mice

2014 ◽  
Vol 221 (3) ◽  
pp. 381-390 ◽  
Author(s):  
Gustavo W Fernandes ◽  
Cintia B Ueta ◽  
Tatiane L Fonseca ◽  
Cecilia H A Gouveia ◽  
Carmen L Lancellotti ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Liver Steatosis ◽  
Mrna Levels ◽  
High Fat ◽  
Adaptive Thermogenesis ◽  
Brown Adipose ◽  
Similar Body

Three types of beta adrenergic receptors (ARβ1–3) mediate the sympathetic activation of brown adipose tissue (BAT), the key thermogenic site for mice which is also present in adult humans. In this study, we evaluated adaptive thermogenesis and metabolic profile of a mouse withArβ2knockout (ARβ2KO). At room temperature, ARβ2KO mice have normal core temperature and, upon acute cold exposure (4 °C for 4 h), ARβ2KO mice accelerate energy expenditure normally and attempt to maintain body temperature. ARβ2KO mice also exhibited normal interscapular BAT thermal profiles during a 30-min infusion of norepinephrine or dobutamine, possibly due to marked elevation of interscapular BAT (iBAT) and ofArβ1, andArβ3mRNA levels. In addition, ARβ2KO mice exhibit similar body weight, adiposity, fasting plasma glucose, cholesterol, and triglycerides when compared with WT controls, but exhibit marked fasting hyperinsulinemia and elevation in hepaticPepck(Pck1) mRNA levels. The animals were fed a high-fat diet (40% fat) for 6 weeks, ARβ2KO mice doubled their caloric intake, accelerated energy expenditure, and inducedUcp1expression in a manner similar to WT controls, exhibiting a similar body weight gain and increase in the size of white adipocytes to the WT controls. However, ARβ2KO mice maintain fasting hyperglycemia as compared with WT controls despite very elevated insulin levels, but similar degrees of liver steatosis and hyperlipidemia. In conclusion, inactivation of the ARβ2KO pathway preserves cold- and diet-induced adaptive thermogenesis but disrupts glucose homeostasis possibly by accelerating hepatic glucose production and insulin secretion. Feeding on a high-fat diet worsens the metabolic imbalance, with significant fasting hyperglycemia but similar liver structure and lipid profile to the WT controls.

scholarly journals Influence of gender on OVA-induced airway inflammation in C57/B6J mice on a high-fat diet

2018 ◽  
Vol 16 ◽  
pp. 205873921876094 ◽  
Author(s):  
Gang Yu ◽  
Lili Zhu ◽  
Haiyan Li ◽  
Youyou Shao ◽  
Lei Chong ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Inflammatory Cells ◽  
Normal Weight ◽  
Male Mice ◽  
High Fat ◽  
Low Fat ◽  
Control Male ◽  
Low Fat Diet ◽  
Asthma Group

Overweight/obesity has been suggested as a risk factor for asthma development, and prospective studies have confirmed that high body weight precedes asthma symptoms. However, the nature of the association between overweight/obese status and asthma remains unclear. Animal models of obesity-related asthma are very useful for understanding disease pathophysiology. Although C57/B6J mice are the most widely used animal model for researching obesity-related asthma, gender differences are not always taken into consideration. Therefore, to explore the effect of gender on the development of obesity-related asthma, both female and male C57/B6J mice were used in this study. The mice were fed with a high-fat diet or a low-fat diet as control. Body weight, body length, liver weight, and Lee’s Index were used to evaluate obesity status, and lung histology, lung inflammatory cells infiltration, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined for asthma evaluation. We found that the mean body weight of male mice on a high-fat diet gradually increased and was significantly higher than control male mice on a low-fat diet ( P < 0.01), while no significant differences were found between female mice at the end of 12 weeks of feeding. Furthermore, the obese asthma group female and male mice exhibited significantly high inflammatory cells infiltration than normal weight or obese female and male mice ( P < 0.01). However, the obese asthma group presented higher Neu infiltration, Th1 cytokine, and interferon gamma (IFNγ) concentrations in BALF than the asthma group in both the genders ( P < 0.01). In conclusion, both female and male mice are suitable for the obesity-related asthma model, although male mice might be more stable. Besides, obesity-related asthma is not Th2 type asthma.

scholarly journals Oat bran β-glucan improves glucose homeostasis in mice fed on a high-fat diet

RSC Advances ◽  
2017 ◽  
Vol 7 (86) ◽  
pp. 54717-54725 ◽  
Author(s):  
Yuliang Cheng ◽  
Jie Zhang ◽  
Kaiyun Luo ◽  
Genyi Zhang
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Oat Bran

The changes of body weight (A) and food intake (B) of mice fed on different diets of low-fat (LF), high-fat (HF), HF + grain form β-glucan (HFGF), and HF + extracted β-glucan (HFEX).

scholarly journals Combination effects of a fatty diet and exercise on the depressive state and cardioprotection in apolipoprotein E knockout mice with a change in RCAN1 expression

2020 ◽  
Vol 48 (11) ◽  
pp. 030006052096401
Author(s):  
Wang Shuo ◽  
Haicong Li ◽  
Nishijo Muneko ◽  
Nishino Yoshikazu ◽  
Nobuo Kato ◽  
...  
Keyword(s):  
Body Weight ◽  
Apolipoprotein E ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Heart Weight ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Apolipoprotein E Knockout Mice ◽  
Diet And Exercise

Objective Regulator of calcineurin 1 (RCAN1) controls plasticity of the nervous system and depressive conditions by regulating brain-derived neurotropic factor (BDNF) and plays a crucial role in neural and cardiac pathways. The apolipoprotein E gene ( ApoE) is a robust risk factor for progression of Alzheimer’s disease. A fatty diet is considered detrimental for metabolic disorders, such as obesity and cardiovascular diseases. Methods We examined the neuronal and cardiac protective roles of RCAN1 in ApoE−/− mice that were fed a high- or low-fat diet with and without voluntary movement for 3 months. Organ weights, laboratory data, histology, RNA expression, and behavior were examined. Results A high-fat diet with exercise improved depressive function, as examined by the forced swimming test, and RCAN1 mRNA expression was induced in the hippocampus. A low-fat diet with exercise resulted in a reduced body weight, higher heart weight/body weight ratio, and lower circulating triglyceride levels compared with a low-fat diet without exercise. RCAN1 mRNA expression was increased in cardiomyocytes in ApoE−/− mice. Conclusions The combination of a high-fat diet and exercise might reduce depressive function, whereas a low-fat diet with exercise leads to cardioprotection. Induction of RCAN1 expression might affect neuroplasticity and cardiac function.

scholarly journals Increased expression of receptors for orexigenic factors in nodose ganglion of diet-induced obese rats

2009 ◽  
Vol 296 (4) ◽  
pp. E898-E903 ◽  
Author(s):  
Gabriel Paulino ◽  
Claire Barbier de la Serre ◽  
Trina A. Knotts ◽  
Pieter J. Oort ◽  
John W. Newman ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Afferent Pathway ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Vagal Afferent

The vagal afferent pathway is important in short-term regulation of food intake, and decreased activation of this neural pathway with long-term ingestion of a high-fat diet may contribute to hyperphagic weight gain. We tested the hypothesis that expression of genes encoding receptors for orexigenic factors in vagal afferent neurons are increased by long-term ingestion of a high-fat diet, thus supporting orexigenic signals from the gut. Obesity-prone (DIO-P) rats fed a high-fat diet showed increased body weight and hyperleptinemia compared with low-fat diet-fed controls and high-fat diet-induced obesity-resistant (DIO-R) rats. Expression of the type I cannabinoid receptor and growth hormone secretagogue receptor 1a in the nodose ganglia was increased in DIO-P compared with low-fat diet-fed controls or DIO-R rats. Shifts in the balance between orexigenic and anorexigenic signals within the vagal afferent pathway may influence food intake and body weight gain induced by high fat diets.

scholarly journals THE ROLE OF THE INTESTINAL MICROBIOTA IN THE MODULATION OF FOOD INTAKE AND BODY WEIGHT

2017 ◽  
Author(s):  
Matthew John Dalby
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Intestinal Microbiota ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Diet Induced Obesity

This research investigated the role of the intestinal microbiota in shaping host food intake and body weight through immunomodulation, the impact of refined and unrefined diets, and though fermentable fibre induced gastrointestinal hormone secretion. Gut-derived lipopolysaccharide activating TLR4 has been proposed to contribute to obesity. To investigate this, TLR4-/- or CD14-/- mice and C57BL/6J controls were fed a high-fat or low-fat diet. Neither TLR4-/- or CD14-/- were protected against high-fat diet-induced obesity. High-fat diet increased hypothalamic expression of SerpinA3N and SOCS3 regardless of genotype; however, inflammatory gene expression was not increased. To investigate the use of chow control diets in obesity-associated microbiota changes, C57BL/6J mice were fed a chow diet, refined high-fat, or low-fat diet. Both high-fat and low-fat refined diets resulted in similar dramatic alterations in the composition of the intestinal microbiota at the phylum, family, and species level compared to chow, while only high-fat diet feeding resulted in obesity and glucose intolerance. The roles of colonic GLP-1 and PYY in mediating fermentable fibre in reducing food intake and body fat were investigated using GLP-1R-/- and PYY-/- mice fed a high-fat diet supplemented with inulin or cellulose. Inulin supplementation reduced body fat and food intake in C57BL/6J control mice while GLP-1R-/- and PYY-/- mice showed an attenuated response to dietary inulin. In summary, this research questions the role of TLR4 and LPS in diet-induced obesity. These results demonstrate the importance of the control diet used in studies of obesity in mice and indicate that many of the obesity-associated changes in the gut microbiota are due to comparing refined high-fat diets with chow diets. These results also provide evidence for an essential role for both GLP-1 and PYY in mediating the food intake and bodyweight-reducing effects of fermentable fibre.

scholarly journals The influence of dietary fat on fat metabolism and body Fat deposition in meal-feeding and nibbling rats

1975 ◽  
Vol 34 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J. D. Wood ◽  
J. T. Reid
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Body Fat ◽  
High Fat Diet ◽  
Fat Metabolism ◽  
Dietary Fatty Acids ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Fat Pads

1. An experiment was done with rats (body-weight 160 g) to study the effects on fat metabolism and body composition of low (10 g/kg)- or high (140 g/kg)-fat diets fed as one meal for one 4 h period/d (meal-feeders) or as six spaced meals/d (nibblers). The daily energy intake/unit metabolic body-weight (body-weight0.73) was the same for all four groups, and this level of intake was about 80% of that consumed by rats allowed unrestricted access to the low-fat diet. The experimental period was 76 d.2. Rats given the high-fat diet deposited more body fat/d and, as a result, grew faster and were energetically more efficient than rats given the low-fat diet. The high-fat diet depressed de novo lipogenesis from glucose in epididymal and perirenal fat pads, whose fatty acid composition resembled that of the diet.3. For both diets meal-feeders had greater stomach plus small intestine weights than nibblers and had higher plasma free fatty acid levels, when they were killed 15 h after their last meal.4. Meal-feeders given the low-fat diet had the greatest rate of lipogenesis for fat pads.5. Meal-feeders given the high-fat diet deposited less of the main dietary fatty acids in their fat pads.6. There was no evidence that meal-feeders eating a high-fat diet adapt their metabolism so completely that they become more efficient utilizers than those nibbling this diet. Meal-feeders eating the low-fat diet became no fatter than nibblers of this diet, possibly because they were eating less than their daily ad lib. intake.

Metformin prevents airway hyperreactivity in rats with dietary obesity

2021 ◽  
Author(s):  
Gina N. Calco ◽  
Becky J. Proskocil ◽  
David B. Jacoby ◽  
Allison D Fryer ◽  
Zhenying Nie
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
High Fat Diet ◽  
Fasting Glucose ◽  
Airway Hyperreactivity ◽  
Male Rats ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Dietary Obesity

Increased insulin is associated with obesity-related airway hyperreactivity and asthma. We tested whether the use of metformin, an anti-diabetic drug used to reduce insulin resistance, can reduce circulating insulin, thereby preventing airway hyperreactivity in rats with dietary obesity. Male and female rats were fed a high- or low-fat diet for 5 weeks. Some male rats were simultaneously treated with metformin (100 mg/kg, p.o.). In separate experiments, after 5 weeks of a high-fat diet, some rats were switched to a low-fat diet, while others continued a high-fat diet for an additional 5 weeks. Bronchoconstriction and bradycardia in response to bilateral electrical vagus nerve stimulation or to inhaled methacholine were measured in anesthetized and vagotomized rats. Body weight, body fat, caloric intake, fasting glucose and insulin were measured. Vagally-induced bronchoconstriction was potentiated only in male rats on a high-fat diet. Males gained more body weight, body fat, and had increased levels of fasting insulin, compared to females. Metformin prevented development of vagally-induced airway hyperreactivity in male rats on high-fat diet, in addition to inhibiting weight gain, fat gain and increased insulin. In contrast, switching rats to a low-fat diet for 5 weeks reduced body weight and body fat, it did not reverse fasting glucose, fasting insulin or potentiation of vagally-induced airway hyperreactivity. These data suggest that medications that target insulin may be effective treatment for obesity-related asthma.

scholarly journals Lipid–zinc interaction: its effect on the testes of mice

1995 ◽  
Vol 73 (5) ◽  
pp. 723-731
Author(s):  
S. K. Taneja ◽  
S. Chadha ◽  
P. Arya
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Giant Cells ◽  
Zn Deficiency ◽  
Testicular Function ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Cholesterol Levels ◽  
Maize Oil

Lipid-Zn interaction in the testes of mice was studied by feeding them low-fat (30 g maize oil/kg; group LFZD) and high-fat (90 g maize oil/kg; group HFZD) Zn-deficient diets for 6 weeks. The results were compared with those of corresponding Zn-supplemented-diet-fed controls (groups LFZS and HFZS). The integument-related Zn-deficiency symptoms appeared in group HFZD and not in group LFZD mice despite lack of Zn in their ration and an equal level of Zn in their blood serum. The feed intake, gain in body weight and testes weight of the LFZD group were comparable with those of the LFZS and HFZS groups (P < 0·05) but were higher than those of the group HFZD (P <·05). The testes of group HFZD displayed necrotic changes marked by the presence of giant cells, lower RNA, DNA and protein concentrations and higher phospholipid and cholesterol levels than those of mice in the LFZD group. The concentrations of these fractions were not significantly different between LFZD and HFZS. The results do not support the hypothesis that Zn is essential either for testicular function or for nucleic acid and protein synthesis in animals fed on a low-fat diet; however, it appears to be essential for animals fed on a high-fat diet. The changes observed in the testes of the HFZD animais suggest the excess intake of fat as their cause in Zn-deficient animals.

scholarly journals The effect of pre-resection obesity on post-resection body composition after 75% small bowel resection in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Neesha S. Patel ◽  
Ujwal R. Yanala ◽  
Shruthishree Aravind ◽  
Roger D. Reidelberger ◽  
Jon S. Thompson ◽  
...  
Keyword(s):  
Body Weight ◽  
Small Bowel ◽  
Lean Mass ◽  
Bowel Resection ◽  
Small Bowel Resection ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Massive Resection ◽  
Obese Rats

AbstractIn patients with short bowel syndrome, an elevated pre-resection Body Mass Index may be protective of post-resection body composition. We hypothesized that rats with diet-induced obesity would lose less lean body mass after undergoing massive small bowel resection compared to non-obese rats. Rats (CD IGS; age = 2 mo; N = 80) were randomly assigned to either a high-fat (obese rats) or a low-fat diet (non-obese rats), and fed ad lib for six months. Each diet group then was randomized to either underwent a 75% distal small bowel resection (massive resection) or small bowel transection with re-anastomosis (sham resection). All rats then were fed ad lib with an intermediate-fat diet (25% of total calories) for two months. Body weight and quantitative magnetic resonance-determined body composition were monitored. Preoperative body weight was 884 ± 95 versus 741 ± 75 g, and preoperative percent body fat was 35.8 ± 3.9 versus 24.9 ± 4.6%; high-fat vs. low fat diet, respectively (p < 0.0001); preoperative diet type had no effect on lean mass. Regarding total body weight, massive resection produced an 18% versus 5% decrease in high-fat versus low-fat rats respectively, while sham resection produced a 2% decrease vs. a 7% increase, respectively (p < 0.0001, preoperative vs. necropsy data). Sham resection had no effect on lean mass; after massive resection, both high-fat and low-fat rats lost lean mass, but these changes were not different between the latter two rat groups. The high-fat diet and low-fat diet induced obesity and marginal obesity, respectively. The massive resection produced greater weight loss in high-fat rats compared to low-fat rats. The type of dietary preconditioning had no effect on lean mass loss after massive resection. A protective effect of pre-existing obesity on lean mass after massive intestinal resection was not demonstrated.

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