scholarly journals Rcan2 and estradiol independently regulate body weight in female mice

Oncotarget ◽  
2017 ◽  
Vol 8 (29) ◽  
pp. 48098-48109 ◽  
Author(s):  
Ling-Cui Ding ◽  
Qian-Qian Gong ◽  
Shi-Wei Li ◽  
Xiao-Long Fu ◽  
Ye-Cheng Jin ◽  
...  
Keyword(s):  
Body Weight ◽  
Female Mice ◽  
Regulate Body Weight

scholarly journals NPY Deficiency Prevents Postmenopausal Adiposity by Augmenting Estradiol-Mediated Browning

2018 ◽  
Vol 75 (6) ◽  
pp. 1042-1049
Author(s):  
Seongjoon Park ◽  
Erkhembayar Nayantai ◽  
Toshimitsu Komatsu ◽  
Hiroko Hayashi ◽  
Ryoichi Mori ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Fat Metabolism ◽  
Male Mice ◽  
Wild Type ◽  
Male And Female ◽  
Female Mice ◽  
Age Related ◽  
Promising Target ◽  
Intracellular Mechanism

Abstract The orexigenic hormone neuropeptide Y (NPY) plays a pivotal role in the peripheral regulation of fat metabolism. However, the mechanisms underlying the effects of sex on NPY function have not been extensively analyzed. In this study, we examined the effects of NPY deficiency on fat metabolism in male and female mice. Body weight was slightly decreased, whereas white adipose tissue (WAT) mass was significantly decreased as the thermogenic program was upregulated in NPY-/- female mice compared with that in wild-type mice; these factors were not altered in response to NPY deficiency in male mice. Moreover, lack of NPY resulted in an increase in luteinizing hormone (LH) expression in the pituitary gland, with concomitant activation of the estradiol-mediated thermogenic program in inguinal WAT, and alleviated age-related modification of adiposity in female mice. Taken together, these data revealed a novel intracellular mechanism of NPY in the regulation of fat metabolism and highlighted the sexual dimorphism of NPY as a promising target for drug development to reduce postmenopausal adiposity.

scholarly journals Effects of Bisphenol-A (BPA) and black seed oil on body weight, lipid profile and serum glucose in male and female mice

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
K. M. Sujan ◽  
E. Haque ◽  
M. S. Rakib ◽  
M. I. Haque ◽  
A. Mustari ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Bisphenol A ◽  
Lipid Profile ◽  
Seed Oil ◽  
Serum Glucose ◽  
Male And Female ◽  
Female Mice ◽  
Black Seed ◽  
Black Seed Oil

Background: Bisphenol-A [BPA, 2, 2-bis (hydroxyphenyl) propane] is widely used in the manufacture of polycarbonate plastic, water bottles, feeders , baby bottles, epoxy resins and inside coating in metallic food cans. Black seed oil (BSO) (Nigella sativa) commonly known as black cumin, reported to be beneficial in function of various systems in the body. The study was carried out to investigate the effect of BPA and BSO on body weight, lipid profile and serum glucose in male and female mice. Methods : A total of thirty (15 male and 15 female) Swiss Albino mice (Mus musculus), aged 25-28 days with an average body weight of 27.4±1g were randomly divided into 3 groups consisting 5 mice in each for each sex. Group A served as vehicle control. Group B was administered BPA @ 50 mg/kg bw daily, while group C received both BPA @ 50 mg/kg/day and BSO @ 1ml/kg/day respectively. Results: Data revealed that BPA treated mice showed slight increase in body weight gain while BSO controlled the weight gain in BPA treated mice. Cholesterol and LDL values were significantly (p<0.01) increased and Triglycerides value was significantly (p<0.01) decreased in BPA-treated mice without significant alterations in HDL value. BPA & BSO treated female mice showed significant (p<0.01) decreased in cholesterol, triglycerides and LDL values. BPA reduced the blood glucose level and addition of BSO had synergistic effects of glucose utilization. Conclusions: It can be concluded that BPA is one of the potential risk factors for hyperlipidemia and obesity. These harmful effects could be alleviated by the ingestion of black seed oil.

scholarly journals Identifying Characteristics of Frailty in Female Mice Using a Phenotype Assessment Tool

2019 ◽  
Vol 75 (4) ◽  
pp. 640-646 ◽  
Author(s):  
Dongmin Kwak ◽  
Cory W Baumann ◽  
LaDora V Thompson
Keyword(s):  
Physical Activity ◽  
Body Weight ◽  
Life Span ◽  
Walking Speed ◽  
Assessment Tool ◽  
Preclinical Studies ◽  
Frailty Phenotype ◽  
Female Mice ◽  
Yield Information ◽  
Underlying Mechanisms

Abstract Preclinical studies are important in identifying the underlying mechanisms contributing to frailty. Frailty studies have mainly focused on male rodents with little directed at female rodents. Therefore, the purposes of this study were to identify the onset and prevalence of frailty across the life span in female mice, and to determine if frailty predicts mortality. Female C57BL/6 (n = 27) mice starting at 17 months of age were assessed across the life span using a frailty phenotype, which included body weight, walking speed, strength, endurance, and physical activity. The onset of frailty occurred at approximately 17 months (1/27 mice), with the prevalence of frailty increasing thereafter. At 17 months, 11.1% of the mice were pre-frail and by 26 months peaked at 36.9%. The percentage of frail mice progressively increased up to 66.7% at 32 months. Non-frail mice lived to 29 months whereas frail/pre-frail mice lived only to 26 months (p = .04). In closing, using a mouse frailty phenotype, we are able to identify that the prevalence of frailty in female mice increases across the life span and accurately predicts mortality. Together, this frailty phenotype has the potential to yield information about the underlying mechanisms contributing to frailty.

ADDITIVE, NONADDITIVE AND MATERNAL GENETIC EFFECTS ON ADIPOSITY IN MICE FED DIFFERENT LEVELS OF FAT

1982 ◽  
Vol 24 (3) ◽  
pp. 347-360 ◽  
Author(s):  
A. de Padua Deodato ◽  
E. J. Eisen ◽  
J. M. Leatherwood
Keyword(s):  
Body Weight ◽  
Dietary Fat ◽  
Subcutaneous Fat ◽  
Genetic Effects ◽  
Major Portion ◽  
Female Mice ◽  
Ad Libitum ◽  
The Difference ◽  
Fat Depot ◽  
Different Levels

Polygenic obese (M16), nonobese (ICR) and reciprocal crossbred (M16 male × ICR female and ICR male × M16 female) mice were fed ad libitum diets containing 1, 5 or 25% fat from 3 to 10 weeks of age. Epididymal and subcutaneous fat depot weights (E, S) and depot weights as a proportion of empty body weight (E%, S%) were used as measures of adiposity at 6 and 10 weeks of age. Genetic differences in adiposity among the four populations were partitioned into average direct (a), average maternal (m) and direct heterotic (h) effects. Line M16 was greater than ICR at both 6 and 10 weeks in E (81% at 6 weeks and 114% at 10 weeks), S (82%, 73%), E% (27%, 37%) and S% (26%, 12%). Average direct genetic effects, as determined by a, accounted for 60% of the M16 vs. ICR line difference in E and S at six weeks, the remainder of the difference being due to m. The major portion of the line difference in E% and S% at 6 weeks was accounted for by m. At ten weeks of age, most of the line difference in E, S, E% and S% was due to additive direct genetic effects while the contribution of maternal genetic effects was negligible. Heterosis was sizeable for all measures of adiposity, varying from 10.8% in S% at 10 weeks to 26.8% in E at six weeks, possibly indicating the presence of directional dominance. E and E% increased significantly with the increase in dietary fat percent, but S and S% were not affected. Interactions of genotype with level of dietary fat percent were not significant for the epididymal or subcutaneous fat depot weights or proportional weights.

scholarly journals Sexually Dimorphic Regulation of Gut Microbiota and Body Weight by a Naturally Occurring Flavonoid

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 472-472
Author(s):  
Priyanka Sharma ◽  
Guojun Wu ◽  
Hong Ye ◽  
Yan Y Lam ◽  
Deeptha Kumaraswamy ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Intestinal Microbiome ◽  
Sexually Dimorphic ◽  
Female Mice ◽  
Diet Induced Obesity ◽  
Naturally Occurring ◽  
Principal Coordinates ◽  
Brown Adipose ◽  
Microbiota Structure

Abstract Objectives 7,8-Dihydroxyflavone (DHF) is a naturally occurring flavonoid that is being actively investigated as a therapeutic modality in the treatment of neurological disorders. A recent study also indicated that oral DHF supplementation protected female but not male mice from diet-induced obesity. However, the mechanisms underlying this sexually-dimorphic effects of DHF were not known. The aim of the work is to investigate the mechanisms underlying sex-specific effects of flavonoid. Methods Age-matched male and female mice were given ad libitum access to high fat-diet and drinking water containing vehicle or DHF for 12 weeks. Body weights, body composition, food, and water intake, were assessed. Immunohistological analysis, immunohistochemistry staining, plasma triglycerides, plasma bile acids, and hepatic lipids were investigated. Fresh fecal samples were collected, genomic DNA was extracted and hypervariable region V4 of the 16S rRNA gene was amplified. Gut microbiota structure was evaluated using alpha diversity indices and beta diversity distance metrices. Principal coordinates analysis (PCoA) was performed using the R “ape” package to visualize differences in gut microbiota structure between treatment groups along principal coordinates that accounted for most of the variations. Results Oral administration of DHF, remodels the intestinal microbiome of female, but not male, prior to divergence in body weight. This is concomitant with increase in brown adipose tissue thermogenesis, mediated by increased expression of UCP1 and Pgc -1α protecting the female mice from diet-induced obesity. Conclusions This study demonstrates sexually-dimorphic effects of a clinically relevant natural compound. Importantly, it points to a role for sex-dependent remodeling of the intestinal microbiome as a mechanism for weight control in females. Thus, our discoveries pave the way for personalized nutrition strategies that account for sex differences in metabolism. Funding Sources NIH.

scholarly journals Postnatal Feeding With a Fat Rich Diet Induces Precocious Puberty Independent of Body Weight, Body Fat, and Leptin Levels in Female Mice

2019 ◽  
Vol 10 ◽  
Author(s):  
Rahim Ullah ◽  
Ali Raza ◽  
Naveed Rauf ◽  
Yi Shen ◽  
Yu-Dong Zhou ◽  
...  
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Precocious Puberty ◽  
Female Mice

scholarly journals Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

2014 ◽  
Vol 220 (3) ◽  
pp. 375-388 ◽  
Author(s):  
Lydie Naulé ◽  
Marie Picot ◽  
Mariangela Martini ◽  
Caroline Parmentier ◽  
Hélène Hardin-Pouzet ◽  
...  
Keyword(s):  
Body Weight ◽  
Sexual Behavior ◽  
Bisphenol A ◽  
Preoptic Area ◽  
Third Ventricle ◽  
Daily Intake ◽  
Maternal Exposure ◽  
Developmental Exposure ◽  
Female Mice ◽  
Reference Doses

Bisphenol A (BPA) is a widespread estrogenic compound. We investigated the effects of maternal exposure to BPA at reference doses on sexual behavior and neuroendocrine functions of female offspring in C57BL/6J mice. The dams were orally exposed to vehicle alone or vehicle-containing BPA at doses equivalent to the no observed adverse effect level (5 mg/kg body weight per day) and tolerable daily intake (TDI, 0.05 mg/kg body weight per day) level from gestational day 15 until weaning. Developmental exposure to BPA increased the lordosis quotient in naive females exposed to BPA at the TDI dose only. BPA exposure had no effect on olfactory preference, ability to express masculine behaviors or number of calbindin-positive cells, a sexually dimorphic population of the preoptic area. BPA at both doses selectively increased kisspeptin cell number in the preoptic periventricular nucleus of the rostral periventricular area of the third ventricle in adult females. It did not affect the number of GNRH-positive cells or percentage of kisspeptin appositions on GNRH neurons in the preoptic area. These changes were associated with higher levels of estradiol (E2) at the TDI dose while levels of LH, estrus cyclicity, ovarian and uterine weights, and fertility remained unaffected. Delay in the time of vaginal opening was observed during the postnatal period at TDI dose, without any alteration in body growth. This shows that developmental exposure to BPA at reference doses did not masculinize and defeminize the neural circuitry underlying sexual behavior in female mice. The TDI dose specifically exacerbated responses normally induced by ovarian E2, through estrogen receptor α, during the postnatal/prepubertal period.

scholarly journals Administration of Saccharin to Neonatal Mice Influences Body Composition of Adult Males and Reduces Body Weight of Females

Endocrinology ◽  
2014 ◽  
Vol 155 (4) ◽  
pp. 1313-1326 ◽  
Author(s):  
Sebastian D. Parlee ◽  
Becky R. Simon ◽  
Erica L. Scheller ◽  
Emilyn U. Alejandro ◽  
Brian S. Learman ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Bone Mass ◽  
Composition Analysis ◽  
Male Body ◽  
Adult Males ◽  
Male Mice ◽  
Female Mice ◽  
Trabecular Bone Mass ◽  
High Concentrations

Nutritional or pharmacological perturbations during perinatal growth can cause persistent effects on the function of white adipose tissue, altering susceptibility to obesity later in life. Previous studies have established that saccharin, a nonnutritive sweetener, inhibits lipolysis in mature adipocytes and stimulates adipogenesis. Thus, the current study tested whether neonatal exposure to saccharin via maternal lactation increased susceptibility of mice to diet-induced obesity. Saccharin decreased body weight of female mice beginning postnatal week 3. Decreased liver weights on week 14 corroborated this diminished body weight. Initially, saccharin also reduced male mouse body weight. By week 5, weights transiently rebounded above controls, and by week 14, male body weights did not differ. Body composition analysis revealed that saccharin increased lean and decreased fat mass of male mice, the latter due to decreased adipocyte size and epididymal, perirenal, and sc adipose weights. A mild improvement in glucose tolerance without a change in insulin sensitivity or secretion aligned with this leaner phenotype. Interestingly, microcomputed tomography analysis indicated that saccharin also increased cortical and trabecular bone mass of male mice and modified cortical bone alone in female mice. A modest increase in circulating testosterone may contribute to the leaner phenotype in male mice. Accordingly, the current study established a developmental period in which saccharin at high concentrations reduces adiposity and increases lean and bone mass in male mice while decreasing generalized growth in female mice.

scholarly journals The effects of physiological adaptations to calorie restriction on global cell proliferation rates

2011 ◽  
Vol 300 (4) ◽  
pp. E735-E745 ◽  
Author(s):  
Matthew D. Bruss ◽  
Airlia C. S. Thompson ◽  
Ishita Aggarwal ◽  
Cyrus F. Khambatta ◽  
Marc K. Hellerstein
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Body Fat ◽  
Calorie Restriction ◽  
Percent Body Fat ◽  
Female Mice ◽  
Physiological Adaptations ◽  
Running Wheels

Calorie restriction (CR) reduces the rate of cell proliferation in mitotic tissues. It has been suggested that this reduction in cell proliferation may mediate CR-induced increases in longevity. However, the mechanisms that lead to CR-induced reductions in cell proliferation rates remain unclear. To evaluate the CR-induced physiological adaptations that may mediate reductions in cell proliferation rates, we altered housing temperature and access to voluntary running wheels to determine the effects of food intake, energy expenditure, percent body fat, and body weight on proliferation rates of keratinocytes, liver cells, mammary epithelial cells, and splenic T-cells in C57BL/6 mice. We found that ∼20% CR led to a reduction in cell proliferation rates in all cell types. However, lower cell proliferation rates were not observed with reductions in 1) food intake and energy expenditure in female mice housed at 27°C, 2) percent body fat in female mice provided running wheels, or 3) body weight in male mice provided running wheels compared with ad libitum-fed controls. In contrast, reductions in insulin-like growth factor I were associated with decreased cell proliferation rates. Taken together, these data suggest that CR-induced reductions in food intake, energy expenditure, percent body fat, and body weight do not account for the reductions in global cell proliferation rates observed in CR. In addition, these data are consistent with the hypothesis that reduced cell proliferation rates could be useful as a biomarker of interventions that increase longevity.

scholarly journals Loss of UCP1 exacerbates Western diet-induced glycemic dysregulation independent of changes in body weight in female mice

2017 ◽  
Vol 312 (1) ◽  
pp. R74-R84 ◽  
Author(s):  
Nathan C. Winn ◽  
Victoria J. Vieira-Potter ◽  
Michelle L. Gastecki ◽  
Rebecca J. Welly ◽  
Rebecca J. Scroggins ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Glucose Intolerance ◽  
Immune Cell ◽  
Uncoupling Protein ◽  
Liver Steatosis ◽  
Western Diet ◽  
Female Mice ◽  
Brown Adipose

We tested the hypothesis that female mice null for uncoupling protein 1 (UCP1) would have increased susceptibility to Western diet-induced “whitening” of brown adipose tissue (AT) and glucose intolerance. Six-week-old C57BL/6J wild-type (WT) and UCP1 knockout (UCP1−/−) mice, housed at 25°C, were randomized to either a control diet (10% kcal from fat) or Western diet (45% kcal from fat and 1% cholesterol) for 28 wk. Loss of UCP1 had no effect on energy intake, energy expenditure, spontaneous physical activity, weight gain, or visceral white AT mass. Despite similar susceptibility to weight gain compared with WT, UCP1−/− exhibited whitening of brown AT evidenced by a striking ~500% increase in mass and appearance of large unilocular adipocytes, increased expression of genes related to inflammation, immune cell infiltration, and endoplasmic reticulum/oxidative stress ( P < 0.05), and decreased mitochondrial subunit protein (COX I, II, III, and IV, P < 0.05), all of which were exacerbated by Western diet ( P < 0.05). UCP1−/− mice also developed liver steatosis and glucose intolerance, which was worsened by Western diet. Collectively, these findings demonstrate that loss of UCP1 exacerbates Western diet-induced whitening of brown AT, glucose intolerance, and induces liver steatosis. Notably, the adverse metabolic manifestations of UCP1−/− were independent of changes in body weight, visceral adiposity, and energy expenditure. These novel findings uncover a previously unrecognized metabolic protective role of UCP1 that is independent of its already established role in energy homeostasis.

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