Reduced meal frequency alleviates high-fat diet-induced lipid accumulation and inflammation in adipose tissue of pigs under the circumstance of fixed feed allowance

Abstract Background: The aim of this study was to investigate the effect of Acer tegmentosum Maxim (ATM) on adipocyte differentiation in 3T3-L1 adipocyte-derived cells and anti-obesity properties in high fat diet (HFD)-induced obese rats. Methods: 3T3-L1 adipocytes and HFD-induced obese rats were treated with ATM, and its effect on gene expression was analyzed using RT-PCR and Western blotting experiments. Results: Cellular lipid contents in DMI (dexamethasone, 3-isobutyl-1-methylxanthine, and insulin mixture)-treated cells increased, while ATM treatment caused a significant reduction in lipid accumulation in differentiated 3T3-L1 cells. ATM caused inhibition of adipogenesis via down-regulation of the CCAAT/enhancer binding protein β (C/EBPβ), C/EBPα, and peroxisome proliferator-activated receptor γ (PPARγ) expressions in 3T3-L1 cells. Moreover, treatment with ATM caused a decrease in the expressions of adipocyte-specific genes, such as adipocyte fatty acid-binding protein-2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL), compared with DMI-stimulated adipocytes. In addition, phosphorylation levels of protein kinase B (Akt) and its downstream substrate, glycogen synthase kinase 3β (GSK3β), were significantly decreased by ATM treatment of 3T3-L1 adipocytes. Together, these results indicated that ATM caused inhibition of both adipocyte differentiation via suppression of the C/EBP family and PPARγ expressions and the Akt signaling pathway in 3T3-L1 adipocytes. In the present study, we further investigated anti-obesity effects of ATM on HFD-induced obese rats. Rats fed with HFD demonstrated elevations in body weight gain, while the administration of ATM significantly reversed BW gains and adipose tissue weights in rats fed HFD. ATM supplementation also caused a decrease in the circulating triglyceride levels and total cholesterol levels and led to inhibition of lipid accumulation in the adipose tissues in HFD-induced obesity in rats. Furthermore, epididymal fat exhibited larger adipocytes in the HFD group, whereas the ATM-treated group was significantly smaller than that of HFD group. These results strongly demonstrate that ATM administration caused a reduction in adiposity via attenuation in adipose tissue mass and adipocyte size. Conclusion: These finding demonstrated that ATM exerted anti-obesity effects through inhibition of adipocyte differentiation and adipogenesis, leading to a decrease in BW and fat tissue mass in HFD-induced obesity in rats.

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A High-Fat Diet Attenuates Amp-Activated Protein Kinase α1 in Adipocytes to Induce Exosome Shedding and Nonalcoholic Fatty Liver Development in Vivo

10.2337/figshare.13259768 ◽

2020 ◽

Author(s):

Ada Admin ◽

Chenghui Yan ◽

Xiaoxiang Tian ◽

Jiayin Li ◽

Dan Liu ◽

...

Keyword(s):

Adipose Tissue ◽

Protein Kinase ◽

Fatty Liver ◽

Lipid Accumulation ◽

High Fat Diet ◽

Liver Development ◽

High Fat ◽

Tissue Specific ◽

Nonalcoholic Fatty Liver ◽

Amp Activated Protein Kinase

Exosomes are important for intercellular communication, but the role of exosomes in the communication between adipose tissue (<a>AT</a>) and the liver remains unknown. The aim of this study is to determine the contribution of AT-derived exosomes in nonalcoholic fatty liver disease (<a>NAFLD</a>). Exosome components, liver fat content, and liver function were monitored in AT in mice fed a <a>high-fat diet </a>(<a>HFD</a>) or treated with metformin- or GW4869 and with AMP-activated protein kinase (AMPKα1) floxed (Prkaα1fl/fl/WT), <a>Prkaα1-/-</a>, liver tissue-specific Prkaα1-/-, or AT-specific Prkaα1-/- modification. In cultured adipocytes and white adipose tissue (WAT), the absence of <a>AMPKα1</a> increased exosome release and exosomal proteins by elevating <a>tumor susceptibility gene 101 (TSG101</a>)-mediated exosome biogenesis. In adipocytes treated with palmitic acid, TSG101 facilitated scavenger receptor class B (CD36) sorting into exosomes. CD36-containing exosomes were then endocytosed by hepatocytes to induce lipid accumulation and inflammation. Consistently, an HFD induced more severe lipid accumulation and cell death in <a>Prkaα1-/- </a>and adipose tissue-specific Prkaα1-/- mice than in WT and liver-specific Prkaα1-/- mice. AMPK activation by metformin reduced adipocyte-mediated exosome release and mitigated fatty liver development in WT and liver specific Prkaα1-/- mice. Moreover, administration of the exosome inhibitor GW4869 blocked exosome secretion and alleviated HFD-induced fatty livers in Prkaα1-/- and adipocyte-specific Prkaα1-/- mice. We conclude that HFD-mediated AMPKα1 inhibition promotes NAFLD by increasing numbers of AT C<a>D36</a>-containing exosomes.

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Emodin inhibits lipid accumulation and inflammation in adipose tissue of high‐fat diet‐fed mice by inducing M2 polarization of adipose tissue macrophages

The FASEB Journal ◽

10.1096/fj.202100157rr ◽

2021 ◽

Vol 35 (7) ◽

Author(s):

Fang Yu ◽

Nan Yu ◽

Jie Peng ◽

Yan Zhao ◽

Lei Zhang ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Accumulation ◽

High Fat Diet ◽

High Fat ◽

M2 Polarization ◽

Adipose Tissue Macrophages

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Dietary diacylglycerol prevents high-fat diet-induced lipid accumulation in rat liver and abdominal adipose tissue

Lipids ◽

10.1007/s11745-004-1199-1 ◽

2004 ◽

Vol 39 (1) ◽

pp. 37-41 ◽

Cited By ~ 87

Author(s):

Xianghe Meng ◽

Dongya Zou ◽

Zhongping Shi ◽

Zouying Duan ◽

Zhonggui Mao

Keyword(s):

Adipose Tissue ◽

Rat Liver ◽

Lipid Accumulation ◽

High Fat Diet ◽

High Fat ◽

Abdominal Adipose Tissue

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Mice lacking PLAP-1/asporin counteracts high fat diet-induced metabolic disorder and alveolar bone loss by controlling adipose tissue expansion

Scientific Reports ◽

10.1038/s41598-021-84512-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Hiromi Sakashita ◽

Satoru Yamada ◽

Masaki Kinoshita ◽

Tetsuhiro Kajikawa ◽

Tomoaki Iwayama ◽

...

Keyword(s):

Adipose Tissue ◽

Periodontal Disease ◽

Lipid Accumulation ◽

High Fat Diet ◽

Periodontal Ligament ◽

Metabolic Disorders ◽

Alveolar Bone ◽

High Fat ◽

Knock Out ◽

Knock Out Mice

AbstractAdipose tissue fibrosis with chronic inflammation is a hallmark of obesity-related metabolic disorders, and the role of proteoglycans in developing adipose tissue fibrosis is of interest. Periodontal disease is associated with obesity; however, the underlying molecular mechanisms remain unclear. Here we investigated the roles of periodontal ligament associated protein-1 (PLAP-1)/asporin, a proteoglycan preferentially and highly expressed in the periodontal ligament, in obesity-related adipose tissue dysfunction and adipocyte differentiation. It was found that PLAP-1 is also highly expressed in white adipose tissues. Plap-1 knock-out mice counteracted obesity and alveolar bone resorption induced by a high-fat diet. Plap-1 knock-down in 3T3-L1 cells resulted in less lipid accumulation, and recombinant PLAP-1 enhanced lipid accumulation in 3T3-L1 cells. In addition, it was found that primary preadipocytes isolated from Plap-1 knock-out mice showed lesser lipid accumulation than the wild-type (WT) mice. Furthermore, the stromal vascular fraction of Plap-1 knock-out mice showed different extracellular matrix gene expression patterns compared to WT. These findings demonstrate that PLAP-1 enhances adipogenesis and could be a key molecule in understanding the association between periodontal disease and obesity-related metabolic disorders.

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Dietary Curcuminoids Prevent High-Fat Diet–Induced Lipid Accumulation in Rat Liver and Epididymal Adipose Tissue

Journal of Nutrition ◽

10.1093/jn/131.11.2932 ◽

2001 ◽

Vol 131 (11) ◽

pp. 2932-2935 ◽

Cited By ~ 133

Author(s):

Akira Asai ◽

Teruo Miyazawa

Keyword(s):

Adipose Tissue ◽

Rat Liver ◽

Lipid Accumulation ◽

High Fat Diet ◽

Epididymal Adipose Tissue ◽

High Fat

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A single day of high fat diet feeding induces lipid accumulation and insulin resistance in brown adipose tissue in mice

Atherosclerosis ◽

10.1016/j.atherosclerosis.2020.10.267 ◽

2020 ◽

Vol 315 ◽

pp. e87

Author(s):

M. Modder ◽

E.N. Kuipers ◽

N.M. Held ◽

W. In Het Panhuis ◽

P.M.M. Ruppert ◽

...

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Brown Adipose Tissue ◽

Lipid Accumulation ◽

High Fat Diet ◽

High Fat ◽

Brown Adipose

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Male and Female Animals Respond Differently to High-Fat Diet and Regular Exercise Training in a Mouse Model of Hyperlipidemia

International Journal of Molecular Sciences ◽

10.3390/ijms22084198 ◽

2021 ◽

Vol 22 (8) ◽

pp. 4198

Author(s):

Melinda E. Tóth ◽

Brigitta Dukay ◽

Mária Péter ◽

Gábor Balogh ◽

Gergő Szűcs ◽

...

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Lipid Accumulation ◽

High Fat Diet ◽

The Body ◽

Treadmill Running ◽

Cardiometabolic Health ◽

Regular Exercise ◽

High Fat ◽

Brown Adipose

Inappropriate nutrition and a sedentary lifestyle can lead to obesity, one of the most common risk factors for several chronic diseases. Although regular physical exercise is an efficient approach to improve cardiometabolic health, the exact cellular processes are still not fully understood. We aimed to analyze the morphological, gene expression, and lipidomic patterns in the liver and adipose tissues in response to regular exercise. Healthy (wild type on a normal diet) and hyperlipidemic, high-fat diet-fed (HFD-fed) apolipoprotein B-100 (APOB-100)-overexpressing mice were trained by treadmill running for 7 months. The serum concentrations of triglyceride and tumor necrosis factor α (TNFα), as well as the level of lipid accumulation in the liver, were significantly higher in HFD-fed APOB-100 males compared to females. However, regular exercise almost completely abolished lipid accumulation in the liver of hyperlipidemic animals. The expression level of the thermogenesis marker, uncoupling protein-1 (Ucp1), was significantly higher in the subcutaneous white adipose tissue of healthy females, as well as in the brown adipose tissue of HFD-fed APOB-100 females, compared to males. Lipidomic analyses revealed that hyperlipidemia essentially remodeled the lipidome of brown adipose tissue, affecting both the membrane and storage lipid fractions, which was partially restored by exercise in both sexes. Our results revealed more severe metabolic disturbances in HFD-fed APOB-100 males compared to females. However, exercise efficiently reduced the body weight, serum triglyceride levels, expression of pro-inflammatory factors, and hepatic lipid accumulation in our model.

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