Differential induction of enzymes and genes involved in lipid metabolism in liver and visceral adipose tissue of juvenile yellow catfish Pelteobagrus fulvidraco exposed to copper

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

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The human type 2 diabetes-specific visceral adipose tissue proteome and transcriptome in obesity

Scientific Reports ◽

10.1038/s41598-021-96995-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Nicholas J. Carruthers ◽

Clarissa Strieder-Barboza ◽

Joseph A. Caruso ◽

Carmen G. Flesher ◽

Nicki A. Baker ◽

...

Keyword(s):

Type 2 Diabetes ◽

Adipose Tissue ◽

Fatty Acid ◽

Lipid Metabolism ◽

Visceral Adipose Tissue ◽

Sequencing Analysis ◽

Complement Factor ◽

Endothelial Protein C Receptor ◽

Visceral Adipose

AbstractDysfunctional visceral adipose tissue (VAT) in obesity is associated with type 2 diabetes (DM) but underlying mechanisms remain unclear. Our objective in this discovery analysis was to identify genes and proteins regulated by DM to elucidate aberrant cellular metabolic and signaling mediators. We performed label-free proteomics and RNA-sequencing analysis of VAT from female bariatric surgery subjects with DM and without DM (NDM). We quantified 1965 protein groups, 23 proteins, and 372 genes that were differently abundant in DM vs. NDM VAT. Proteins downregulated in DM were related to fatty acid synthesis and mitochondrial function (fatty acid synthase, FASN; dihydrolipoyl dehydrogenase, mitochondrial, E3 component, DLD; succinate dehydrogenase-α, SDHA) while proteins upregulated in DM were associated with innate immunity and transcriptional regulation (vitronectin, VTN; endothelial protein C receptor, EPCR; signal transducer and activator of transcription 5B, STAT5B). Transcriptome indicated defects in innate inflammation, lipid metabolism, and extracellular matrix (ECM) function, and components of complement classical and alternative cascades. The VAT proteome and transcriptome shared 13 biological processes impacted by DM, related to complement activation, cell proliferation and migration, ECM organization, lipid metabolism, and gluconeogenesis. Our data revealed a marked effect of DM in downregulating FASN. We also demonstrate enrichment of complement factor B (CFB), coagulation factor XIII A chain (F13A1), thrombospondin 1 (THBS1), and integrins at mRNA and protein levels, albeit with lower q-values and lack of Western blot or PCR confirmation. Our findings suggest putative mechanisms of VAT dysfunction in DM.

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Expression of LONP1 Is High in Visceral Adipose Tissue in Obesity, and Is Associated with Glucose and Lipid Metabolism

Endocrinology and Metabolism ◽

10.3803/enm.2021.1023 ◽

2021 ◽

Author(s):

Ju Hee Lee ◽

Saet-Byel Jung ◽

Seong Eun Lee ◽

Ji Eun Kim ◽

Jung Tae Kim ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

Visceral Adipose Tissue ◽

Glucose And Lipid Metabolism ◽

Visceral Adipose

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Adaptation of AMPK-mTOR-signal pathways and lipid metabolism in response to low- and high-rapeseed meal diet in Chinese perch (Siniperca chuatsi)

10.21203/rs.3.rs-17136/v1 ◽

2020 ◽

Author(s):

Jiao Li ◽

Xu-Fang Liang ◽

Muhammad Shoaib Alam ◽

Haocan Luo ◽

Yanpeng Zhang ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

Growth Performance ◽

Mrna Expression ◽

Visceral Adipose Tissue ◽

Rapeseed Meal ◽

Whole Body ◽

Signal Pathways ◽

Chinese Perch ◽

Visceral Adipose

Abstract Background: Chinese perch, a carnivorous fish, can accept artificial diet after domestication nowadays, and this farm way will gain high economic interest and sustainability. However, the high content and high quality requirement of dietary protein make it need the high cost in Chinese perch. Therefore, the aim of this study was to explore the effect of fish meal replacement by low- or high-rapeseed meal on growth performance, feeding, lipid and glucose metabolism. Methods: Three experimental diets were formulated with 0, 10% and 30% rapeseed meal, named as control, RSL and RSH, groups respectively. After the 8-week of feeding trial, growth performance, lipid metabolism and AMPK-mTOR-signal pathways were measured. Results: Chinese perch fed with RSH and RSL diets showed significantly decreased WG, SGR, BFR, VSI, MSI and the whole-body crude lipid compared to those fed with the control diet (P < 0.05). Fish in RSL group decreased feed intake, serum LDL-C, hepatic mRNA expression of LPL, PEPCK and phosphorylated Grb10 (P < 0.05). In visceral adipose tissue, mRNA expression of FAS, SREBP1, ACC1, HL, CPT1 and PEPCK were all significantly down-regulated (P < 0.05). Fish in RSH group showed phosphorylated AMPK, hepatic mRNA expression of SREBP1, ACC1, FAS, PPARα and CPT1 were down-regulated, while HSL, G6PD and PC were up-regulated (P < 0.05). In visceral adipose tissue, mRNA expressions of SREBP1, LPL, CPT1 and PEPCK were down-regulated, while mRNA expression of HSL was up-regulated (P < 0.05). Conclusions: Chinese perch fed with RSL and RSH diets showed decreased fat deposition in viscera. Fish fed with low level of rapeseed meal diet ate less diet, which caused inhibited lipid metabolism in the liver and visceral adipose tissues.Fish fed with high level of rapeseed meal diet inhibited hepatic FA synthesis, activated lipolysis, hence reducing Acetyl-CoA pool. In turn, β-oxidation were inhibited, glycolysis was activated, thus lipid accumulation was decreased. In visceral adipose tissue, lipid uptake was inhibited, caused inhibited FA synthesis, β-oxidation, glycerol synthesis, and improved lipolysis.

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Protein Metabolism in Human Obesity: Relationship with Glucose and Lipid Metabolism and with Visceral Adipose Tissue

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.82.8.2552 ◽

1997 ◽

Vol 82 (8) ◽

pp. 2552-2558 ◽

Cited By ~ 14

Author(s):

A. Solini

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

Visceral Adipose Tissue ◽

Protein Metabolism ◽

Human Obesity ◽

Glucose And Lipid Metabolism ◽

Visceral Adipose

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Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2018.04.015 ◽

2018 ◽

Vol 476 ◽

pp. 110-118 ◽

Cited By ~ 5

Author(s):

Biljana Bursać ◽

Ana Djordjevic ◽

Nataša Veličković ◽

Danijela Vojnović Milutinović ◽

Snježana Petrović ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

Chronic Stress ◽

Visceral Adipose Tissue ◽

Tissue Lipid ◽

High Fructose Diet ◽

High Fructose ◽

Visceral Adipose

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Removal of Epididymal Visceral Adipose Tissue Prevents Obesity-Induced Multi-organ Insulin Resistance in Male Mice

Journal of the Endocrine Society ◽

10.1210/jendso/bvab024 ◽

2021 ◽

Vol 5 (5) ◽

Author(s):

Michael P Franczyk ◽

Mai He ◽

Jun Yoshino

Keyword(s):

Insulin Resistance ◽

Skeletal Muscle ◽

Adipose Tissue ◽

Lipid Metabolism ◽

Visceral Adipose Tissue ◽

Body Weight Gain ◽

Whole Body ◽

Atherogenic Dyslipidemia ◽

Glucose And Lipid Metabolism ◽

Visceral Adipose

Abstract Obesity is associated with insulin resistance, an important risk factor of type 2 diabetes, atherogenic dyslipidemia, and nonalcoholic fatty liver disease. The major purpose of this study was to test hypothesize that prophylactic removal of epididymal visceral adipose tissue (VAT) prevents obesity-induced multi-organ (liver, skeletal muscle, adipose tissue) insulin resistance. Accordingly, we surgically removed epididymal VAT pads from adult C57BL/6J mice and evaluated in vivo and cellular metabolic pathways involved in glucose and lipid metabolism following chronic high-fat diet (HFD) feeding. We found that VAT removal decreases HFD-induced body weight gain while increasing subcutaneous adipose tissue (SAT) mass. Strikingly, VAT removal prevents obesity-induced insulin resistance and hyperinsulinemia and markedly enhances insulin-stimulated AKT-phosphorylation at serine-473 (Ser473) and threonine-308 (Thr308) sites in SAT, liver, and skeletal muscle. VAT removal leads to decreases in plasma lipid concentrations and hepatic triglyceride (TG) content. In addition, VAT removal increases circulating adiponectin, a key insulin-sensitizing adipokine, whereas it decreases circulating interleukin 6, a pro-inflammatory adipokine. Consistent with these findings, VAT removal increases adenosine monophosphate–activated protein kinase C phosphorylation, a major downstream target of adiponectin signaling. Data obtained from RNA sequencing suggest that VAT removal prevents obesity-induced oxidative stress and inflammation in liver and SAT, respectively. Taken together, these findings highlight the metabolic benefits and possible action mechanisms of prophylactic VAT removal on obesity-induced insulin resistance and hepatosteatosis. Our results also provide important insight into understanding the extraordinary capability of adipose tissue to influence whole-body glucose and lipid metabolism as an active endocrine organ.

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