Thermoneutrality attenuates body weight gain in ovariectomized female mice

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Ashley R. Chandler ◽  
Michelina M. Messina ◽  
J. Michael Overton
Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 150-158 ◽  
Author(s):  
Liangru Zhu ◽  
Yongjie Yang ◽  
Pingwen Xu ◽  
Fang Zou ◽  
Xiaofeng Yan ◽  
...  

2006 ◽  
Vol 290 (1) ◽  
pp. G36-G48 ◽  
Author(s):  
Gregory G. Martin ◽  
Barbara P. Atshaves ◽  
Avery L. McIntosh ◽  
John T. Mackie ◽  
Ann B. Kier ◽  
...  

Although liver fatty acid binding protein (L-FABP) is postulated to influence cholesterol homeostasis, the physiological significance of this hypothesis remains to be resolved. This issue was addressed by examining the response of young (7 wk) female mice to L-FABP gene ablation and a cholesterol-rich diet. In control-fed mice, L-FABP gene ablation alone induced hepatic cholesterol accumulation (2.6-fold), increased bile acid levels, and increased body weight gain (primarily as fat tissue mass). In cholesterol-fed mice, L-FABP gene ablation further enhanced the hepatic accumulation of cholesterol (especially cholesterol ester, 12-fold) and potentiated the effects of dietary cholesterol on increased body weight gain, again mainly as fat tissue mass. However, in contrast to the effects of L-FABP gene ablation in control-fed mice, biliary levels of bile acids (as well as cholesterol and phospholipids) were reduced. These phenotypic alterations were not associated with differences in food intake. In conclusion, it was shown for the first time that L-FABP altered cholesterol metabolism and the response of female mice to dietary cholesterol. While the biliary and lipid phenotype of female wild-type L-FABP+/+ mice was sensitive to dietary cholesterol, L-FABP gene ablation dramatically enhanced many of the effects of dietary cholesterol to greatly induce hepatic cholesterol (primarily cholesterol ester) and triacylglycerol accumulation as well as to potentiate body weight gain (primarily as fat tissue mass). Taken together, these data support the hypothesis that L-FABP is involved in the physiological regulation of cholesterol metabolism, body weight gain, and obesity.


Endocrinology ◽  
2021 ◽  
Author(s):  
Caroline M Ancel ◽  
Maggie C Evans ◽  
Romy I Kerbus ◽  
Elliot G Wallace ◽  
Greg M Anderson

Abstract Reproductive dysfunction in women has been linked to high calorie diet (HCD)-feeding and obesity. Central resistance to leptin and insulin have been shown to accompany diet-induced infertility in rodent studies, and we have previously shown that deleting suppressor of cytokine signaling 3, which is a negative regulator of leptin signaling, from all forebrain neurons partially protects mice from HCD-induced infertility. In this study, we were interested in exploring the role of protein tyrosine phosphatase 1B (PTP1B), which is a negative regulator of both leptin and insulin signaling, in the pathophysiology of HCD-induced obesity and infertility. To this end, we generated male and female neuron-specific PTP1B knockout mice and compared their body weight gain, food intake, glucose tolerance and fertility to control littermates under both normal calorie diet-feeding and HCD-feeding conditions. Both male and female mice with neuronal PTP1B deletion exhibited slower body weight gain in response to HCD-feeding, yet only male knockout mice exhibited improved glucose tolerance compared with controls. Neuronal PTP1B deletion improved the time to first litter in HCD-fed mice, but did not protect female mice from eventual HCD-induced infertility. While the mice fed a normal caloric diet remained fertile throughout the 150 day period of assessment, HCD-fed females became infertile after producing only a single litter, regardless of their genotype. These data show that neuronal PTP1B deletion is able to partially protect mice from HCD-induced obesity, but is not a critical mediator of HCD-induced infertility.


2021 ◽  
Author(s):  
Isao Tamura ◽  
Hiroshi Tamura ◽  
Mai Kawamoto-Jozaki ◽  
Yumiko Doi-tanaka ◽  
Haruka Takagi ◽  
...  

Women usually experience body weight gain with aging, which can put them at risk for many chronic diseases. Previous studies indicated that melatonin treatment attenuates body weight gain and abdominal fat deposition in several male animals. However, it is unclear whether melatonin affects female animals in the same way. This study investigated whether long-term melatonin treatment can attenuate body weight gain with aging and, if it does, what the mechanism is. Ten-week-old female ICR mice were given melatonin-containing water (100 μg/mL) or water only until 43 weeks. Melatonin treatment significantly attenuated body weight gain at 23 weeks (control; 57.2±2.0 g vs. melatonin; 44.4±3.1 g), 33 weeks (control; 65.4±2.6 g vs. melatonin; 52.2±4.2 g) and 43 weeks (control; 66.1±3.2 g vs. melatonin; 54.4±2.5 g) without decreasing the amount of food intake. Micro-CT analyses showed that melatonin significantly decreased the deposition of visceral and subcutaneous fat. These results suggested that melatonin attenuates body weight gain by inhibiting abdominal fat deposition. Metabolome analysis of the liver revealed that melatonin treatment induced a drastic change in the metabolome with the down-regulation of 149 metabolites, including the metabolites of glucose and amino acids. Citrate, which serves as a source of de novo lipogenesis, was one of the down-regulated metabolites. These results show that long-term melatonin treatment induces drastic changes of metabolism and attenuates body weight gain and fat deposition with aging in female mice.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mohammed A Khan ◽  
Preethi Samuel ◽  
Sourashish Nag ◽  
Tahir Hussain

Obesity in itself is a disease condition and a major risk factor in the development of hypertension, dyslipidemia, and hyperglycemia. Therefore, successful strategies for improving obesity and related metabolic risk factors are needed. Role of renin-angiotensin system (RAS) has been implicated in obesity and metabolic dysfunction. Recently, we have shown that AT2R knock-out in female mice caused a greater body weight gain and hyperinsulimia in response to high fat diet (HFD). In the present study, we hypothesize that AT2R activation rescues diet-induced obesity in females. To test this hypothesis, we injected AT2R non-peptide agonist C21 (0.3mg/kg/day i.p) in C57BL6 female mice on HFD for 12 weeks. C21-treatment did not affect the HFD calorie intake (HFD: 937±18 Kcal; C21HFD: 886±37 Kcal) but caused lesser body weight gain compared to control (HFD: 4.4± 0.4g; C21HFD: 3.06± 0.4g). Similar to the body weight gain pattern, gonadal fat weight and adipocyte size were decreased significantly in C21-treated mice on HFD compared to control HFD group (HFD: 4.4± 0.4 g; C21 HFD: 3.06± 0.4g) and (HFD: 6404±161.6μm2 ; C21HFD: 3874±103.2μm2 ) respectively. Moreover, the C21-treated females on HFD had lower levels of plasma insulin, improved glucose tolerance, and decreased plasma free fatty acids and hepatic triglycerides. Western blot revealed that phospho-Ser79-acetyl CoA carboxylase (p-Ser79-ACC-1) was reduced, an index of increased lipogenic activity and decreased β-oxidation process, in both adipose (Adi) and hepatic (Hep) tissues of HFD fed groups (Adi: 86% and Hep: 73% of 100% controls); C21-treatment revered the decrease in p-ser79-ACC-1 in Adi (104% of control) and caused an increase in Hep (122% of control) respectively. The HFD feeding lowered the estradiol level (ND: 38.8±2.6 vs HFD:11.3±1.2ng), which was modestly reversed by C21 treatment (C21HFD:17.4± 1.5ng) in HFD mice. Our results strongly suggest that stimulation of AT2R in female mice positively contribute, predominantly independent of estrogen, to rescue body weight gain and adipocyte size increase in response to HFD. We propose reduced lipogenesis and enhanced lipid β-oxidation as potential mechanisms linked to AT2R action in reducing obesity and its related metabolic disorders in females.


2017 ◽  
Vol 25 (2) ◽  
pp. 193-207
Author(s):  
Song Young Baek ◽  
Hye Rim Lee ◽  
Ju Hye Park ◽  
Michung Yoon ◽  
Yoosik Yoon ◽  
...  

2018 ◽  
Vol 16 (2) ◽  
pp. 201-210
Author(s):  
Muryanto Muryanto ◽  
Pita Sudrajad ◽  
Amrih Prasetyo

The aim of the study was to determine the development of ramie plants (Boehmeria nivea L. Gaud) and the effect of using ramie leaves on feed on the body weight gain of Wonosobo Sheep (Dombos). Research on the development of ramie plants using survey methods in the area of ramie plant development in Wonosobo Regency. While the research on the use of ramie leaves for fattening was carried out in Butuh Village, Kalikajar District, Wonosobo Regency in 2018. 21 male Dombos were divided into 3 feed treatments with forage proportions of 70%, 50% and 30 ramie leaves respectively. %. The results showed that currently ramie plants were being developed in Wonosobo Regency by CV. Ramindo Berkah Persada Sejahtera in Gandok Village, Kalikajar District, Wonosobo Regency, Central Java. Until now the area of the crop has reached 13 ha. Of this area will produce ramie leaves 195,000 kg / year. If one sheep needs 4 kg of ramie / tail / day leaves, then the potential capacity of sheep is 135 heads / year, if the given one is 50% then the Jurnal Litbang Provinsi Jawa Tengah, Volume 16 202 Nomor 2 – Desember 2018potential capacity is 270 heads / year and if it is reduced again to 25% of ramie leaves then the potential capacity 440 heads / year. The use of ramie leaves as a feed for Wonosobo Sheep fattening can be given as much as 30% in fresh form.


2010 ◽  
Vol 15 (4) ◽  
pp. 262-266 ◽  
Author(s):  
Won-Hee Choi ◽  
Ji-Yun Ahn ◽  
Sun-A Kim ◽  
Tae-Wan Kim ◽  
Tae-Youl Ha

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