Compared to casein, bovine lactoferrin reduces plasma leptin and corticosterone and affects hypothalamic gene expression without altering weight gain or fat mass in high fat diet fed C57/BL6J mice

A variety of natural products have been explored for their antiobesity potential and widely used to develop dietary supplements for the prevention of weight gain from excess body fat. In an attempt to find a natural antiobesity agent, this study was designed to evaluate the antiobesity activity of a novel herbal formulation LI85008F composed of extracts from three medicinal plants in high-fat diet- (HFD-) induced obese mice. After the thirteen-week oral administration of the test materials to mice, the body weight gain, whole-body fat mass, adipose tissue weight, and the expression levels of obesity-related proteins were measured. Our results indicated that LI85008F can suppress body weight gain and lower whole-body fat mass in HFD-induced obese mice. Significant decreases in epididymal and retroperitoneal fat mass were observed in LI85008F-treated groups compared with the HFD-fed control group ( p < 0.05 ). Furthermore, the oral administration of LI85008F caused significant decreases in the expression level of adipogenic (C/EBPα and PPARγ) and lipogenic (ACC) markers and notable increases in the production level of thermogenetic (AMPKα, PGC1α and UCP1) and lipolytic (HSL) proteins. These findings suggest that LI85008F holds great promise for a novel herbal formulation with antiobesity activities, preventing body fat accumulation and altering lipid metabolism.

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Abstract 17361: How Leptin Harms the Heart in High Fat Diet-Induced Obesity

Circulation ◽

10.1161/circ.142.suppl_3.17361 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Maria Pini

Keyword(s):

Body Weight ◽

Mass Loss ◽

Fat Mass ◽

High Fat Diet ◽

Cardiac Fibroblasts ◽

High Fat ◽

Wide Range ◽

Plasma Leptin ◽

Fat Mass Loss

Introduction: Sedentary lifestyle and excessive calorie intake are risk factors for CVD. We have demonstrated the cardioprotective effect of exercise in aged mice and the critical role of visceral adiposity and its profibrotic secretome in increasing cardiovascular risks in obesity and aging. The association between exercise, lowered plasma leptin and reduced inflammatory leukocytes has been recently shown in patients with atherosclerosis. It remains unclear whether elevated plasma leptin can preserve or alter cardiovascular function in obesity. Methods: We analyzed the effect of high fat diet (HFD) in C57BL/6J male mice on the heart in terms of function, structure, histology and key molecular markers. Two interventions were used: 1) active fat mass loss via exercise (daily swimming) during HFD; 2) passive fat mass loss via surgical removal of the visceral adipose tissue (VAT lipectomy) followed by HFD. Results: HFD increased body weight and adiposity, leading to higher plasma leptin, glucose and insulin levels, compared to control diet (CD) mice. HFD impaired left ventricle (LV) structure (hypertrophy, interstitial fibrosis) and cardiac function (echocardiography, in vivo hemodynamics). Atria of HFD mice had enhanced pro-inflammatory protein production. Exercise reduced circulating leptin levels in HFD mice by 50%, in line with fat mass loss. In contrast, lipectomy reduced visceral fat mass, but body weight, adiposity and plasma leptin did not change. Both exercise and VAT lipectomy improved cardiac contractility, reversed collagen deposition and oxidative stress in HFD mice. Both interventions downregulated LV pro-inflammatory markers. We proved the role of leptin in cardiac remodeling in vitro by incubating primary cardiac fibroblasts with hyperleptinemic plasma from HFD mice. Remarkably, plasma from HFD-EX (exercise) suppressed the fibro-proliferative and pro-inflammatory responses of cardiac fibroblasts. Conclusions: Leptin directly contribute to cardiac fibrosis in obesity via activation and proliferation of cardiac fibroblasts. Understanding how leptin signals to the heart might have implications in a wide range of CVD, potentially helping early stratification and personalized care.

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Adipose depot-specific modulation of angiotensinogen gene expression in diet-induced obesity

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00551.2003 ◽

2004 ◽

Vol 286 (6) ◽

pp. E891-E895 ◽

Cited By ~ 64

Author(s):

Kamal Rahmouni ◽

Allyn L. Mark ◽

William G. Haynes ◽

Curt D. Sigmund

Keyword(s):

Gene Expression ◽

Adipose Tissue ◽

High Fat Diet ◽

Rnase Protection Assay ◽

Regulatory Sequences ◽

High Fat ◽

Rnase Protection ◽

Brown Adipose ◽

Normal Chow ◽

Plasma Leptin

Adipose tissue represents an important source of angiotensinogen (AGT). We investigated the effect of obesity induced by a high-fat diet on the expression of mouse (mAGT) and human AGT (hAGT) genes in liver, kidney, and heart and different adipose depots in normal mice (C57BL/6J), and in transgenic mice expressing the hAGT gene under the control of its own promoter. Mice were fed a high-fat diet (45% kcal) or normal chow (10% kcal) for 10 and 20 wk. The expression of mAGT and hAGT mRNA was quantified using an RNAse protection assay. Mice on the high-fat diet exhibited increased weight, fat mass, and plasma leptin. Expression of mAGT or hAGT genes was not affected by high-fat diet in nonadipose tissues, brown adipose tissue, or subcutaneous white fat. In contrast, high-fat diet increased both mAGT and hAGT gene expression in visceral adipose depots (omental, reproductive, and perirenal fat). Thus obesity-induced by a high-fat diet is associated with a tissue-specific increased expression of both mouse and human AGT genes in intra-abdominal adipose tissue. Our findings also suggest that 1.2 kb of regulatory sequences present in the hAGT transgene are sufficient to transcriptionally respond to a high-fat diet in an adipose-specific and depot-specific manner.

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HOX-7 suppresses body weight gain and adipogenesis-related gene expression in high-fat-diet-induced obese mice

BMC Complementary and Alternative Medicine ◽

10.1186/1472-6882-14-505 ◽

2014 ◽

Vol 14 (1) ◽

Cited By ~ 4

Author(s):

Heon-Myung Lee ◽

Hong-Kun Rim ◽

Jong-Hwan Seo ◽

Yoon-Bum Kook ◽

Sung-Kew Kim ◽

...

Keyword(s):

Gene Expression ◽

Body Weight ◽

Weight Gain ◽

High Fat Diet ◽

Body Weight Gain ◽

Obese Mice ◽

Related Gene ◽

High Fat

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

Current Developments in Nutrition ◽

10.1093/cdn/nzab041_018 ◽

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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Four-Week Consumption of Malaysian Honey Reduces Excess Weight Gain and Improves Obesity-Related Parameters in High Fat Diet Induced Obese Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/1342150 ◽

2017 ◽

Vol 2017 ◽

pp. 1-9 ◽

Cited By ~ 17

Author(s):

Suhana Samat ◽

Francis Kanyan Enchang ◽

Fuzina Nor Hussein ◽

Wan Iryani Wan Ismail

Keyword(s):

Weight Gain ◽

High Fat Diet ◽

Physicochemical Analysis ◽

Excess Weight ◽

Sprague Dawley ◽

High Fat ◽

Excess Weight Gain ◽

Sprague Dawley Rats ◽

Acacia Honey ◽

Plasma Leptin

Many studies revealed the potential of honey consumption in controlling obesity. However, no study has been conducted using Malaysian honey. In this study, we investigated the efficacy of two local Malaysian honey types: Gelam and Acacia honey in reducing excess weight gain and other parameters related to obesity. The quality of both honey types was determined through physicochemical analysis and contents of phenolic and flavonoid. Male Sprague-Dawley rats were induced to become obese using high fat diet (HFD) prior to introduction with/without honey or orlistat for four weeks. Significant reductions in excess weight gain and adiposity index were observed in rats fed with Gelam honey compared to HFD rats. Moreover, levels of plasma glucose, triglycerides, and cholesterol, plasma leptin and resistin, liver enzymes, renal function test, and relative organ weight in Gelam and Acacia honey treated groups were reduced significantly when compared to rats fed with HFD only. Similar results were also displayed in rats treated with orlistat, but with hepatotoxicity effects. In conclusion, consumption of honey can be used to control obesity by regulating lipid metabolism and appears to be more effective than orlistat.

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Long-Term Supplementation With Fruits and Vegetables Curbs High-Fat Diet/Obesity-Induced Changes in Body Composition and Favorably Affects Blood T Cell Phenotype in Mice

Current Developments in Nutrition ◽

10.1093/cdn/nzab061_010 ◽

2021 ◽

Vol 5 (Supplement_2) ◽

pp. 1126-1126

Author(s):

Weimin Guo ◽

Dayong Wu ◽

Lijun Li ◽

Edwin Ortega ◽

Yankun Liu ◽

...

Keyword(s):

Body Composition ◽

Body Weight ◽

Weight Gain ◽

T Cell ◽

Fat Mass ◽

High Fat Diet ◽

Cd4 Cells ◽

High Fat ◽

Cell Profile

Abstract Objectives Obesity is associated with impaired immune function. However, impact of obesity on blood T cell profile is not well studied. The objectives of this study were to investigate the effects of high fat diet (HFD)-induced obesity and long-term fruits and vegetable (FV) consumption on body composition and blood T cell profile. Methods This is partial report from an ongoing study. A total of 240 male C57BL/6J mice were randomly assigned to 4 groups: low fat control (LF-C) or high-fat control (HF-C) diet alone, or together with 15% of a unique mixture of FV (w/w, equivalent to 7–9 servings F&V/d for human) (LF-FV or HF-FV). The feeding will continue until 50% mortality is reached in one group. Body weight, body composition (using MRI), and blood T cell profile (using FACS) are monitored longitudinally at different time points. The results reported here are those assessed when mice were 7 months old. Results After 7 months of feeding, mice fed HF-C gained more weight compared to those fed LF-C. Mice fed HF-FV or LF-FV diets had significantly reduced weight gain and fat mass, and higher muscle mass compared to those fed HF-C or LF-C diet, respectively. Mice fed HF-C also had significantly lower percentage of blood CD3+, CD4+, and CD8 + T cells compared with the LF-C. FV supplementation prevented HFD-induced decrease in percentage of CD3+ and CD4+ cells. Furthermore, both % CD3+ and CD4+ cells were negatively correlated with body weight (P < 0.001) or percentage of fat mass (P < 0.001), and positively associated with percentage of lean mass (P < 0.001). Conclusions Our results suggest that consuming large amounts of a unique mixture of F&V curbs HFD-induced body weight gain, reduces fat mass, and favorably affects blood T cell population. Ongoing studies will assess these analytes when mice are 16 months old, and again when one group reaches 50% mortality, and determine their correlations with functional measures of T cell response, host resistance to infection, health span, and mortality. Funding Sources This study was supported by the U.S. Department of Agriculture – Agricultural Research Service (ARS), under Agreement No. 58–1950-4–004.

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Reduced Body Fat and Epididymal Adipose Apelin Expression Associated With Raspberry Ketone [4-(4-Hydroxyphenyl)-2-Butanone] Weight Gain Prevention in High-Fat-Diet Fed Mice

Frontiers in Physiology ◽

10.3389/fphys.2021.771816 ◽

2021 ◽

Vol 12 ◽

Author(s):

Lihong Hao ◽

Nicholas T. Bello

Keyword(s):

Gene Expression ◽

Weight Gain ◽

High Fat Diet ◽

The United States ◽

Metabolic Effects ◽

Control Group ◽

Oral Glucose ◽

High Fat ◽

Oral Gavage ◽

Raspberry Ketone

Raspberry ketone [4-(4-hydroxyphenyl)-2-butanone] is a natural aromatic compound found in raspberries and other fruits. Raspberry ketone (RK) is synthetically produced for use as a commercial flavoring agent. In the United States and other markets, it is sold as a dietary supplement for weight control. The potential of RK to reduce or prevent excessive weight gain is unclear and could be a convergence of several different actions. This study sought to determine whether acute RK can immediately delay carbohydrate hyperglycemia and reduce gastrointestinal emptying. In addition, we explored the metabolic signature of chronic RK to prevent or remedy the metabolic effects of diet-induced weight gain. In high-fat diet (HFD; 45% fat)-fed male mice, acute oral gavage of RK (200 mg/kg) reduced hyperglycemia from oral sucrose load (4 g/kg) at 15 min. In HFD-fed female mice, acute oral RK resulted in an increase in blood glucose at 30 min. Chronic daily oral gavage of RK (200 mg/kg) commencing with HFD access (HFD_RK) for 11 weeks resulted in less body weight gain and reduced fat mass compared with vehicle treated (HFD_Veh) and chronic RK starting 4 weeks after HFD access (HFD_RKw4) groups. Compared with a control group fed a low-fat diet (LFD; 10% fat) and dosed with vehicle (LFD_Veh), glucose AUC of an oral glucose tolerance test was increased with HFD_Veh, but not in HFD_RK or HFD_RKw4. Apelin (Apln) gene expression in epididymal white adipose tissue was increased in HFD_Veh, but reduced to LFD_Veh levels in the HFD_RK group. Peroxisome proliferator activated receptor alpha (Ppara) gene expression was increased in the hepatic tissue of HFD_RK and HFD_RKw4 groups. Overall, our findings suggest that long term daily use of RK prevents diet-induced weight gain, normalizes high-fat diet-induced adipose Apln, and increases hepatic Ppara expression.

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Lactobacillus reuteri improves gut barrier function and affects diurnal variation of the gut microbiota in mice fed a high-fat diet

Food & Function ◽

10.1039/c9fo00417c ◽

2019 ◽

Vol 10 (8) ◽

pp. 4705-4715 ◽

Cited By ~ 5

Author(s):

Shuangqi Li ◽

Ce Qi ◽

Hualing Zhu ◽

Renqiang Yu ◽

Chunliang Xie ◽

...

Keyword(s):

Gene Expression ◽

Weight Gain ◽

Gut Microbiota ◽

Diurnal Variation ◽

High Fat Diet ◽

Serum Lipid ◽

Lactobacillus Reuteri ◽

Mucosal Barrier ◽

High Fat ◽

Gut Barrier Function

Lactobacillus reuteri FN041 prevented HFD induced over weight gain, fat accumulation, endotoxaemia and mucosal-barrier damage, which is related to modulation of diurnal variation of serum lipid, hepatic Fas gene expression, diversity and metabolic activity of gut microbiota.

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Potential probiotic Bifidobacterium animalis ssp. lactis 420 prevents weight gain and glucose intolerance in diet-induced obese mice

Beneficial Microbes ◽

10.3920/bm2014.0014 ◽

2014 ◽

Vol 5 (4) ◽

pp. 437-445 ◽

Cited By ~ 65

Author(s):

L.K. Stenman ◽

A. Waget ◽

C. Garret ◽

P. Klopp ◽

R. Burcelin ◽

...

Keyword(s):

Weight Gain ◽

Glucose Tolerance ◽

Glucose Intolerance ◽

Fat Mass ◽

High Fat Diet ◽

Separate Experiment ◽

Target Tissue ◽

Diabetic Mice ◽

High Fat ◽

Bifidobacterium Animalis

Alterations of the gut microbiota and mucosal barrier are linked with metabolic diseases. Our aim was to investigate the potential benefit of the potential probiotic Bifidobacterium animalis ssp. lactis 420 in reducing high-fat diet-induced body weight gain and diabetes in mice. In the obesity model, C57Bl/6J mice were fed a high-fat diet (60 energy %) for 12 weeks, and gavaged daily with B. lactis 420 (109 cfu) or vehicle. In the diabetes model, mice were fed a high-fat, ketogenic diet (72 energy % fat) for 4 weeks, with a 6-week subsequent treatment with B. lactis 420 (108-1010 cfu/day) or vehicle, after which they were analysed for body composition. We also analysed glucose tolerance, plasma lipopolysaccharide and target tissue inflammation using only one of the B. lactis 420 groups (109 cfu/day). Intestinal bacterial translocation and adhesion were analysed in a separate experiment using an Escherichia coli gavage. Body fat mass was increased in both obese (10.7±0.8 g (mean ± standard error of mean) vs. 1.86±0.21 g, P<0.001) and diabetic mice (3.01±0.4 g vs. 1.14±0.15 g, P<0.001) compared to healthy controls. Treatment with B. lactis 420 significantly decreased fat mass in obese (7.83 ± 0.67 g, P=0.007 compared to obese with vehicle) and diabetic mice (1.89 ± 0.16 g, P=0.02 for highest dose). This was reflected as reduced weight gain and improved glucose tolerance. Furthermore, B. lactis 420 decreased plasma lipopolysaccharide levels (P<0.001), liver inflammation (P=0.04), and E. coli adhesion in the distal gut (P<0.05). In conclusion, B. lactis 420 reduces fat mass and glucose intolerance in both obese and diabetic mice. Reduced intestinal mucosal adherence and plasma lipopolysaccharide suggest a mechanism related to reduced translocation of gut microbes.

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