Acute effects of a high-fat diet on estrous cycling and body weight of intact female mice

2021 ◽  
Author(s):  
Melissa E. Lenert ◽  
Michael D. Burton
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Acute Effects ◽  
High Fat ◽  
Intact Female ◽  
Female Mice ◽  
Estrous Cycling

scholarly journals Tpcn2 knockout mice have improved insulin sensitivity and are protected against high-fat diet-induced weight gain

2018 ◽  
Vol 50 (8) ◽  
pp. 605-614
Author(s):  
Hong He ◽  
Katie Holl ◽  
Sarah DeBehnke ◽  
Chay Teng Yeo ◽  
Polly Hansen ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Wild Type ◽  
High Fat ◽  
Male And Female ◽  
Female Mice

Type 2 diabetes is a complex disorder affected by multiple genes and the environment. Our laboratory has shown that in response to a glucose challenge, two-pore channel 2 ( Tpcn2) knockout mice exhibit a decreased insulin response but normal glucose clearance, suggesting they have improved insulin sensitivity compared with wild-type mice. We tested the hypothesis that improved insulin sensitivity in Tpcn2 knockout mice would protect against the negative effects of a high fat diet. Male and female Tpcn2 knockout (KO), heterozygous (Het), and wild-type (WT) mice were fed a low-fat (LF) or high-fat (HF) diet for 24 wk. HF diet significantly increases body weight in WT mice relative to those on the LF diet; this HF diet-induced increase in body weight is blunted in the Het and KO mice. Despite the protection against diet-induced weight gain, however, Tpcn2 KO mice are not protected against HF-diet-induced changes in glucose or insulin area under the curve during glucose tolerance tests in female mice, while HF diet has no significant effect on glucose tolerance in the male mice, regardless of genotype. Glucose disappearance during an insulin tolerance test is augmented in male KO mice, consistent with our previous findings suggesting enhanced insulin sensitivity in these mice. Male KO mice exhibit increased fasting plasma total cholesterol and triglyceride concentrations relative to WT mice on the LF diet, but this difference disappears in HF diet-fed mice where there is increased cholesterol and triglycerides across all genotypes. These data demonstrate that knockout of Tpcn2 may increase insulin action in male, but not female, mice. In addition, both male and female KO mice are protected against diet-induced weight gain, but this protection is likely independent from glucose tolerance, insulin sensitivity, and plasma lipid levels.

scholarly journals The Influence of High-Fat Diet in Early Life on Intestinal Tumorigenesis in APC1638N Mice

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 272-272
Author(s):  
Ting-Chun Lin ◽  
Ying Tang ◽  
Soonkyu Chung ◽  
Young-Cheul Kim ◽  
Zhenhua Liu
Keyword(s):  
Body Weight ◽  
Wnt Signaling ◽  
Tumor Size ◽  
High Fat Diet ◽  
Early Life ◽  
The Body ◽  
Tumor Incidence ◽  
High Fat ◽  
Intestinal Tumorigenesis ◽  
Female Mice

Abstract Objectives Colorectal cancer (CRC) is one of the most prevalent cancer worldwide. Evidence from epidemiological studies shows that the incidence rate of CRC among elders with age ≥ 50 years is gradually decreased, whereas the rate continuously rise in adults with age < 50 years. Along with the rise of CRC in young adults, a significantly increasing trend in obesity is also observed in youth. The present study aims to investigate how the early-life nutrition influences the intestinal tumorigenesis later in mouse with an age equivalent to an age < 50 years in human. Methods APC1638N mice (4 weeks of age) were fed a low-fat diet (N = 22; LF: 10% kcal from fat) or a high-fat diet (N = 23; HF: 60% kcal from fat) for 8 weeks, which is equivalent to child/adolescent age in humans. After that, all animals were switched to standard chow diet (LabDiet #5P76) and fed for additional 12 weeks before sacrifice. Tumors were examined and the expression tumorigenic Wnt-signaling downstream genes (Cyclin D1, c-Myc and Axin 2) in the intestine were assessed. Results Our results showed that compared to LF group, the body weight of both male and female mice significantly increased after 8-week HF feeding (P < 0.05). After switching to the standard chow diet for further 12 weeks feeding, the increase of body weight in HF group remained, although the degree of magnitude reduced, and a statistical significance only shown in female mice (P < 0.05). There were a higher tumor incidence (P = 0.051) and tumor multiplicity (P < 0.05) in males than female.  No interactions between gender and diet were observed. The HF group had a higher tumor incidence (P = 0.088) and tumor size (P < 0.05) when compared to the LF group. The expression of Wnt-signaling downstream gene, c-Myc, was significantly increased in the HF group at 24-week of age (P < 0.01). Conclusions A short term of high-fat diet in early life tends to promote intestinal tumorigenesis in adults as indicated by a mild increase in tumor incidence and a significant increase in tumor size. Funding Sources This project was supported by the US Department of Agriculture Hatch funding (#1013548).

scholarly journals Replacing Part of Glucose with Galactose in the Postweaning Diet Protects Female But Not Male Mice from High-Fat Diet–Induced Adiposity in Later Life

2019 ◽  
Vol 149 (7) ◽  
pp. 1140-1148 ◽  
Author(s):  
Lianne M S Bouwman ◽  
José M S Fernández-Calleja ◽  
Inge van der Stelt ◽  
Annemarie Oosting ◽  
Jaap Keijer ◽  
...  
Keyword(s):  
Body Weight ◽  
Insulin Receptor ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Later Life ◽  
Partial Replacement ◽  
Model Assessment ◽  
High Fat ◽  
Female Mice ◽  
Subcutaneous White Adipose Tissue

ABSTRACT Background Duration of breastfeeding is positively associated with decreased adiposity and increased metabolic health in later life, which might be related to galactose. Objective The aim of this study was to investigate if partial replacement of glucose with galactose in the postweaning diet had a metabolic programming effect. Methods Male and female mice (C57BL/6JRccHsd) received an isocaloric diet (16 energy% fat; 64 energy% carbohydrates; 20 energy% protein) with either glucose (32 energy%) (GLU) or glucose + galactose (GLU + GAL, 16 energy% each) for 3 wk postweaning. Afterwards, all mice were switched to the same 40 energy% high-fat diet (HFD) for 9 wk to evaluate potential programming effects in an obesogenic environment. Data were analyzed within sex. Results Female body weight (−14%) and fat mass (−47%) were significantly lower at the end of the HFD period (both P < 0.001) among those fed GLU + GAL than among those fed GLU; effects in males were in line with these findings but nonsignificant. Food intake was affected in GLU + GAL–fed females (+8% on postweaning diet, −9% on HFD) compared with GLU-fed females, but not for hypothalamic transcript levels at endpoint. Also, in GLU + GAL–fed females, serum insulin concentrations (−48%, P  < 0.05) and the associated homeostasis model assessment of insulin resistance (HOMA-IR) were significantly lower ( P < 0.05) at endpoint, but there were no changes in pancreas morphology. In GLU + GAL–fed females, expression of insulin receptor substrate 2 (Irs2) (−27%, P  < 0.01 ; −44%, P  < 0.001) and the adipocyte size markers leptin (Lep) (−40%, P  < 0.05; −63% , P  < 0.05) and mesoderm-specific transcript homolog protein (Mest) (−80%, P < 0.05; −72%, P  < 0.05) was lower in gonadal and subcutaneous white adipose tissue (WAT), respectively. Expression of insulin receptor substrate1 (Irs1) (−24%, P  < 0.05) was only lower in subcutaneous WAT in GLU + GAL–fed females. Conclusions Partial replacement of glucose with galactose, resulting in a 1:1 ratio mimicking lactose, in a 3-wk postweaning diet lowered body weight, adiposity, HOMA-IR, and expression of WAT insulin signaling in HFD-challenged female mice in later life. This suggests that prolonged galactose intake may improve metabolic and overall health in later life.

Abstract MP27: Adipose-derived Human Soluble (Pro)renin Receptor Causes Resistance To Losartan Treatment In High-Fat Diet Male And Female Mice

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Kellea Nichols ◽  
Audrey Poupeau ◽  
Eva Gatineau ◽  
Gertrude Arthur ◽  
Frederique B Yiannikouris
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
High Fat Diet ◽  
Partial Agonist ◽  
High Fat ◽  
Male And Female ◽  
Female Mice ◽  
Critical Gap ◽  
Prorenin Receptor ◽  
Obesity Hypertension

Obesity, affecting more that 37% of the US, contributes to hypertension. Despite the use of one or more anti-hypertensive treatments, 48% of the hypertensive population remains with resistant hypertension, which prompts the development for new therapeutic targets. We demonstrated that obesity increased the expression of prorenin receptor (PRR) in the adipose tissue and elevated plasma soluble PRR (sPRR). In addition, the infusion of mouse sPRR increased blood pressure in male mice fed high fat-diet (HF); indicating that adipose-derived sPRR could increase circulating sPRR and contribute to hypertension. However, there is a critical gap in the functional role of human sPRR in obesity-hypertension. In this study, we aim to define whether adipose-derived human sPRR contributes to obesity-hypertension. Human sPRR-Myc-tag transgenic mice were bred with mice expressing adiponectin/Cre to selectively express human sPRR in adipocytes (adi-HsPRR). Adi-HsPRR and control littermate (CTL) male and female mice were fed HF-diet for 20 weeks (N=8-15/group). Body weight was assessed weekly and body composition monthly. Blood pressure was measured by telemetry after 15 weeks of diet. Adipose-derived human sPRR did not significantly elevate body weight or fat mass (Male: CTL.18.3±1.0g; adi-HsPRR. 17.5±0.8g. Female: CTL. 15.6±1.5g; adi-HsPRR. 11.9±1.3g; p>0.05). Systolic blood pressure (SBP) significantly increased in HF-fed male and female mice however; adipose-derived human sPRR did not further elevate SBP (24h SBP. Male: CTL. 136.0±1.7 mmHg; adi-HsPRR: 133.4±1.5mmHg; Female: CTL. 131.9±2.8 mmHg; adi-HsPRR: 130.6±3.1 mmHg; p>0.05). Surprisingly, the anti-hypertensive effect of losartan (Los) to lower blood pressure was significantly reduced in adi-HsPRR male and female mice (Male: CTL. ΔSBP: -12.1±1.5 ΔmmHg; adi-HsPRR: -7.8±0.6 ΔmmHg; Female: CTL. ΔSBP: -13.4±1.1 ΔmmHg; adi-HsPRR: -5.7±2.3 ΔmmHg; p<0.05). In 3T3-L1 cells, sPRR significantly increased phosphorylation of ERK1/2, which was not completely blunted by Los indicating that human sPRR could act as a partial agonist of AT1R or activate ERK1/2 independently of AT1R. Our data suggests that adipose-derived sPRR does not stimulate AT1R-mediated contractility, instead impairs Los efficacy.

scholarly journals Dietary Genistein Could Modulate Hypothalamic Circadian Entrainment, Reduce Body Weight, and Improve Glucose and Lipid Metabolism in Female Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Liyuan Zhou ◽  
Xinhua Xiao ◽  
Qian Zhang ◽  
Jia Zheng ◽  
Ming Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Energy Intake ◽  
High Fat Diet ◽  
High Fat ◽  
Female Mice ◽  
Reduce Body Weight ◽  
Glucose And Lipid Metabolism

Genistein has beneficial effects on metabolic disorders. However, the specific mechanism is not clearly understood. In light of the significant role of the hypothalamus in energy and metabolic homeostasis, this study was designed to explore whether dietary genistein intake could mitigate the harmful effects of a high-fat diet on glucose and lipid metabolism and whether any alterations caused by dietary genistein were associated with hypothalamic gene expression profiles. C57BL/6 female mice were fed a high-fat diet without genistein (HF), a high-fat diet with genistein (HFG), or a normal control diet (CON) for 8 weeks. Body weight and energy intake were assessed. At the end of the study, glucose tolerance and serum levels of insulin and lipids were analyzed. Hypothalamic tissue was collected for whole transcriptome sequencing and reverse transcription quantitative PCR (RT-qPCR) validation. Energy intake and body weight were significantly reduced in the mice of the HFG group compared with those of the HF group. Mice fed the HFG diet had improved glucose tolerance and decreased serum triacylglycerol, free fatty acids, and low-density lipoprotein cholesterol compared with those fed the HF diet. The HFG diet also modulated gene expression in the hypothalamus; the most abundant genes were enriched in the circadian entrainment pathway. Dietary genistein intake could reduce body weight, improve glucose and lipid metabolism, and regulate hypothalamic circadian entrainment. The ability of genistein intake to influence regulation of the hypothalamic circadian rhythm is important since this could provide a novel target for the treatment of obesity and diabetes.

Abstract 75: Chronic Treatment With At2 Receptor Agonist Rescues High Fat Diet-induced Obesity in Female Mice.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mohammed A Khan ◽  
Preethi Samuel ◽  
Sourashish Nag ◽  
Tahir Hussain
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
The Body ◽  
Calorie Intake ◽  
Adipocyte Size ◽  
High Fat ◽  
Female Mice ◽  
Diet Induced Obesity

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.

scholarly journals Characterizing the Retinal Phenotype in the High-Fat Diet and Western Diet Mouse Models of Prediabetes

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 464 ◽  
Author(s):  
Bright Asare-Bediako ◽  
Sunil Noothi ◽  
Sergio Li Calzi ◽  
Baskaran Athmanathan ◽  
Cristiano Vieira ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Fundus Photography ◽  
Vascular Density ◽  
Sensitivity Index ◽  
High Fat ◽  
Permeability Studies ◽  
Induced Changes ◽  
Acellular Capillaries

We sought to delineate the retinal features associated with the high-fat diet (HFD) mouse, a widely used model of obesity. C57BL/6 mice were fed either a high-fat (60% fat; HFD) or low-fat (10% fat; LFD) diet for up to 12 months. The effect of HFD on body weight and insulin resistance were measured. The retina was assessed by electroretinogram (ERG), fundus photography, permeability studies, and trypsin digests for enumeration of acellular capillaries. The HFD cohort experienced hypercholesterolemia when compared to the LFD cohort, but not hyperglycemia. HFD mice developed a higher body weight (60.33 g vs. 30.17g, p < 0.0001) as well as a reduced insulin sensitivity index (9.418 vs. 62.01, p = 0.0002) compared to LFD controls. At 6 months, retinal functional testing demonstrated a reduction in a-wave and b-wave amplitudes. At 12 months, mice on HFD showed evidence of increased retinal nerve infarcts and vascular leakage, reduced vascular density, but no increase in number of acellular capillaries compared to LFD mice. In conclusion, the HFD mouse is a useful model for examining the effect of prediabetes and hypercholesterolemia on the retina. The HFD-induced changes appear to occur slower than those observed in type 2 diabetes (T2D) models but are consistent with other retinopathy models, showing neural damage prior to vascular changes.

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