The effects of high‐fat diet feeding over generations on body fat accumulation associated with lipoprotein lipase and leptin in rat adipose tissues

The factors that control fat deposition in adipose tissues are poorly understood. It is known that visceral adipose tissues display a range of biochemical properties that distinguish them from adipose tissues of subcutaneous origin. However, we have little information on gene expression, either in relation to fat deposition or on interspecies variation in fat deposition. The first step in this study was to identify genes expressed in fat depot of cattle using the differential display RT-PCR method. Among the transcripts identified as having differential expression in the two adipose tissues were cell division cycle 42 homolog (CDC42), prefoldin-5, decorin, phosphate carrier, 12S ribosomal RNA gene, and kelch repeat and BTB domain containing 2 (Kbtbd2). In subsequent experiments, we determined the expression levels of these latter genes in the pig and in mice fed either a control or high-fat diet to compare the regulation of fat accumulation in other animal species. The levels of CDC42 and decorin mRNA were found to be higher in visceral adipose tissue than in subcutaneous adipose tissue in cattle, pig, and mice. However, the other genes studied did not show consistent expression patterns between the two tissues in cattle, pigs, and mice. Interestingly, all genes were upregulated in subcutaneous and/or visceral adipose tissues of mice fed the high-fat diet compared with the control diet. The data presented here extend our understanding of gene expression in fat depots and provide further proof that the mechanisms of fat accumulation differ significantly between animal species.

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Loss of Selenoprotein V Predisposes Mice to Body Fat Accumulation (OR11-02-19)

Current Developments in Nutrition ◽

10.1093/cdn/nzz044.or11-02-19 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Author(s):

Lingli Chen ◽

Jiaqiang Huang ◽

Yuanyuan Wu ◽

Fazheng Ren ◽

Xin Gen Lei

Keyword(s):

Gene Expression ◽

Body Fat ◽

High Fat Diet ◽

The Body ◽

High Fat ◽

Fat Accumulation ◽

Diet Induced Obesity ◽

Body Weights ◽

Its Gene ◽

Selenoprotein V

Abstract Objectives Metabolic function of selenoprotein V (SELENOV) remains unknown, although we previously showed a strong correlation of its gene expression with the high-fat diet-induced obesity in pigs. This study was conducted to explore the role and mechanism of SELENOV in body fat metabolism. Methods We applied the CRISPR/Cas9 gene-targeting deletion to generate Selenovknockout (KO) mice (C57BL/6 J background). Male KO and their wild-type (WT) (8 weeks old, n = 10 per genotype by treatment group) were fed a normal diet (NF, 10% calories coming from fat) or a high-fat diet (HF, 60% calories coming from fat) for 27 weeks. At the end, body weights and composition of mice were recorded, and tissues were collected to assay for gene expression and protein production related to lipid metabolism. Results Body weights of the KO mice fed the NF or HF diet were 16–19% higher (P < 0.05) than those of the WT mice. Total fat mass of the KO mice was 54% higher (P < 0.05) than the WT mice fed either diet, whereas total lean mass of the KO mice was 5 and 35% lower (P < 0.05) than that of WT mice fed the NF and HF diets, respectively. Gene expression of key enzymes (Fasn, Acaca, Dgat1, and Lpl) involved in lipogenesis was elevated (P < 0.05) in the white adipose tissue of the KO mice compared with the WT mice. In contrast, differences in gene expression of enzymes related to lipolysis and fatty acid oxidation (Atgl, Hsl, Ces1d, and Cpt1a) between the two genotypes were exactly the opposite (P < 0.05). Consistently, levels of proteins related to lipid accumulation (pACC, ACC, FAS, and LPL) were upregulated (P < 0.05) and proteins related to lipolysis (ATGL, HSL, and pHSL) were down-regulated (P < 0.05) in the KO mice compared with the WT mice. Conclusions Knockout of Selenov predisposed the male mice to elevated lipogenesis and attenuated lipolyis, leading to the body fat accumulation. This illustrated role and mechanism of SELENOV helps explain our previously-reported correlation between its gene expression and the high-fat diet-induced obesity in pigs. Funding Sources This research was supported in part by a NSFC grant #31,320,103,920.

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Coffee polyphenols suppress diet-induced body fat accumulation by downregulating SREBP-1c and related molecules in C57BL/6J mice

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00441.2010 ◽

2011 ◽

Vol 300 (1) ◽

pp. E122-E133 ◽

Cited By ~ 130

Author(s):

Takatoshi Murase ◽

Koichi Misawa ◽

Yoshihiko Minegishi ◽

Masafumi Aoki ◽

Hideo Ominami ◽

...

Keyword(s):

Body Fat ◽

High Fat Diet ◽

Active Form ◽

Pyruvate Dehydrogenase Kinase ◽

Liver Fat ◽

Mrna Levels ◽

Acetyl Coa Carboxylase ◽

High Fat ◽

Acetyl Coa ◽

Fat Accumulation

The prevalence of obesity is increasing globally, and obesity is a major risk factor for type 2 diabetes and cardiovascular disease. We investigated the effects of coffee polyphenols (CPP), which are abundant in coffee and consumed worldwide, on diet-induced body fat accumulation. C57BL/6J mice were fed either a control diet, a high-fat diet, or a high-fat diet supplemented with 0.5 to 1.0% CPP for 2–15 wk. Supplementation with CPP significantly reduced body weight gain, abdominal and liver fat accumulation, and infiltration of macrophages into adipose tissues. Energy expenditure evaluated by indirect calorimetry was significantly increased in CPP-fed mice. The mRNA levels of sterol regulatory element-binding protein (SREBP)-1c, acetyl-CoA carboxylase-1 and -2, stearoyl-CoA desaturase-1, and pyruvate dehydrogenase kinase-4 in the liver were significantly lower in CPP-fed mice than in high-fat control mice. Similarly, CPP suppressed the expression of these molecules in Hepa 1–6 cells, concomitant with an increase in microRNA-122. Structure-activity relationship studies of nine quinic acid derivatives isolated from CPP in Hepa 1–6 cells suggested that mono- or di-caffeoyl quinic acids (CQA) are active substances in the beneficial effects of CPP. Furthermore, CPP and 5-CQA decreased the nuclear active form of SREBP-1, acetyl-CoA carboxylase activity, and cellular malonyl-CoA levels. These findings indicate that CPP enhances energy metabolism and reduces lipogenesis by downregulating SREBP-1c and related molecules, which leads to the suppression of body fat accumulation.

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NO-1886 (ibrolipim), a lipoprotein lipase activator, increases the expression of uncoupling protein 3 in skeletal muscle and suppresses fat accumulation in high-fat diet–induced obesity in rats

Metabolism ◽

10.1016/j.metabol.2005.06.005 ◽

2005 ◽

Vol 54 (12) ◽

pp. 1587-1592 ◽

Cited By ~ 14

Author(s):

Masataka Kusunoki ◽

Kazuhiko Tsutsumi ◽

Koshi Iwata ◽

Weidong Yin ◽

Takao Nakamura ◽

...

Keyword(s):

Skeletal Muscle ◽

Lipoprotein Lipase ◽

High Fat Diet ◽

Uncoupling Protein ◽

High Fat ◽

Fat Accumulation ◽

Diet Induced Obesity ◽

Uncoupling Protein 3

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Supplementation of Non-Dairy Creamer-Enriched High-Fat Diet with D-Allulose Ameliorated Blood Glucose and Body Fat Accumulation in C57BL/6J Mice

Applied Sciences ◽

10.3390/app9132750 ◽

2019 ◽

Vol 9 (13) ◽

pp. 2750 ◽

Cited By ~ 1

Author(s):

Ga Young Do ◽

Eun-Young Kwon ◽

Yun Jin Kim ◽

Youngji Han ◽

Seong-Bo Kim ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

Blood Glucose ◽

Body Fat ◽

High Fat Diet ◽

Fasting Blood Glucose ◽

Control Group ◽

High Fat ◽

Food Component ◽

Fat Accumulation

D-allulose, which has 70% of the sweet taste of sucrose but nearly no calories, has been reported to inhibit the absorption of lipids and suppress body weight gain in obese mice. Fats in non-dairy creamer consist of highly saturated fatty acids, which can cause various lipid disorders when consumed over a long period. We investigated whether D-allulose supplementation alleviates the effects of a non-dairy creamer-enriched high-fat diet on lipid metabolism. High-fat diets enriched with non-dairy creamer were administered to C57BL/6J mice with or without D-allulose supplementation for eight weeks by the pair-feeding design. Lipid metabolic markers were compared between the non-dairy creamer control group (NDC) and non-dairy creamer allulose group (NDCA). Body, adipose tissue, and liver weights, and fasting blood glucose levels, were significantly lower in the NDCA group than in the NDC group. Fecal fatty acid and triglyceride levels were significantly higher in the NDCA group than in the NDC group. Supplementing a non-dairy creamer-enriched high-fat diet with D-allulose improved overall lipid metabolism, including the plasma and hepatic lipid profiles, hepatic and adipose tissue morphology, and plasma inflammatory adipokine levels in mice. These results suggest that D-allulose can be used as a functional food component for preventing body fat accumulation from a high-fat diet that includes hydrogenated plant fats.

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Lipoprotein lipase in white and brown adipose tissues of exercised rats fed a high-fat diet

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.255.2.r226 ◽

1988 ◽

Vol 255 (2) ◽

pp. R226-R231

Author(s):

Y. Deshaies ◽

J. Arnold ◽

J. Lalonde ◽

D. Richard

Keyword(s):

Adipose Tissue ◽

Exercise Training ◽

Lipoprotein Lipase ◽

Lipase Activity ◽

High Fat Diet ◽

Stock Diet ◽

Lipoprotein Lipase Activity ◽

High Fat ◽

Adipose Tissues ◽

Brown Adipose

The combined effects of a high-fat-supplemented diet and exercise training on serum lipids as well as on lipoprotein lipase activity in white and brown adipose tissues of the rat were evaluated. Male Wistar rats were fed ad libitum either a stock diet or the stock diet supplemented with food items rich in fat. Half of each dietary group was submitted to daily treadmill running for 35 days. Food intake and final body weight were raised by the high-fat-supplemented diet and lowered by exercise training. Postprandial serum triglycerides were not affected by diet or exercise, whereas the latter decreased total cholesterol in the high-fat group only (14%, P less than 0.01). Total lipoprotein lipase activity in white adipose tissue was elevated (120%, P less than 0.01) by high-fat feeding, and this increase was greatly reduced by concomitant exercise training. In brown adipose tissue, however, the large elevation (104%, P less than 0.01) in enzyme activity brought by the high-fat diet was unaltered by concomitant training. Thus a high-fat-supplemented diet increased lipoprotein lipase activity in both an energy-storing and a heat-producing tissue, and exercise training was able to counteract this effect in white, but not in brown, adipose tissue. These findings support the notion that the regulation of lipoprotein lipase is tissue specific.

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Cajanolactone A, a Stilbenoid From Cajanus canjan (L.) Millsp, Prevents High-Fat Diet-Induced Obesity via Suppressing Energy Intake

Frontiers in Pharmacology ◽

10.3389/fphar.2021.695561 ◽

2021 ◽

Vol 12 ◽

Author(s):

Zhuohui Luo ◽

Jiawen Huang ◽

Zhiping Li ◽

Zhiwen Liu ◽

Linchun Fu ◽

...

Keyword(s):

Adipose Tissue ◽

Energy Intake ◽

White Adipose Tissue ◽

High Fat Diet ◽

Drug Candidate ◽

High Fat ◽

Adipose Tissues ◽

Fat Accumulation ◽

Diet Induced Obesity ◽

Brown Adipose

Cajanolactone A (CLA) is a stilbenoid isolated from Cajanus canjan (L.) Millsp with the potential to prevent postmenopausal obesity. In this study, the effect of CLA on high-fat diet (HFD)-induced obesity in female C57BL/6 mice was investigated. It was found that, treatment with CLA reduced the energy intake and effectively protected the mice from HFD-induced body weight gain, fat accumulation within the adipose tissues and liver, and impairment in energy metabolism. Further investigation revealed that CLA significantly down-regulated the expression of ORX, ORXR2, pMCH, and Gal in the hypothalamus and antagonized HFD-induced changes in the expression of UCP1, Pgc-1α, Tfam, and Mfn1 in the inguinal white adipose tissue (iWAT); Caveolin-1, MT and UCP3 in the perigonadal white adipose tissue (pWAT); and Pdhb, IRS2, Mttp, Hadhb, and Cpt1b in the liver. CLA also protected the pWAT and liver from HFD-induced mitochondrial damage. However, neither HFD nor CLA showed an effect on the mass of brown adipose tissue (BAT) or the expression of UCP1 in the BAT. In summary, our findings suggest that CLA is a potential drug candidate for preventing diet-induced obesity, at least in females. CLA works most likely by suppressing the hypothalamic expression of orexigenic genes, which leads to reduced energy intake, and subsequently, reduced fat accumulation, thereby protecting the adipose tissues and the liver from lipid-induced mitochondrial dysfunction.

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