scholarly journals Synergetic Action of Forskolin and Mevastatin Induce Normalization of Lipids Profile in Dyslipidemic Rats through Adenosine Monophosphate Kinase Upregulation

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Aaser M. Abdelazim ◽  
Tamer Ahmed Ismail ◽  
Mosleh M. Abumaghaid ◽  
Islam M. Saadaldin
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Lipid Profile ◽  
Mrna Expression ◽  
Synergetic Effect ◽  
Adenosine Monophosphate ◽  
Hormone Sensitive Lipase ◽  
Albino Rats ◽  
Omental Adipose Tissue ◽  
Triton Wr 1339

In the present study, we examined the synergetic effect of forskolin and mevastatin administration on lipid profile and lipid metabolism in omental adipose tissue in dyslipidemic rats. The study was conducted on forty male albino rats. The rats were randomly classified into four main groups of ten animals in each group as follows: group A, served as control nontreated; group B, rats that received Triton WR 1339 (500 mg/kg); group C, rats that received Triton WR 1339 with forskolin (100% FSK extract 0.5 mg/kg/day) for four weeks; and group D, dyslipidemic rats received both mevastatin and forskolin. At the end of the experimental period, blood and omental adipose tissue samples were collected, preserved, and used for biochemical determination of lipid profile and mRNA expression profile of adenylate cyclase (AC), hormone-sensitive lipase, respectively (HSL), and adenosine monophosphate-activated protein kinase (AMPK). The results showed a significant decline in the serum concentration of total cholesterol, LDL-cholesterol, and triglycerides, although there was a significant increase in serum levels of HDL-cholesterol and glycerol in rats received forskolin alone or with mevastatin when compared with control and dyslipidemic groups. The mRNA expression levels of AC, HSL, and AMPK were significantly increased in omental adipose tissue of rats received forskolin when compared with other groups. In conclusion, forskolin acts synergistically with mevastatin to lower lipid profile and improve lipid metabolism in dyslipidemic rats through upregulation of AMPK expression.

scholarly journals Orexin receptor expression in human adipose tissue: effects of orexin-A and orexin-B

2006 ◽  
Vol 191 (1) ◽  
pp. 129-136 ◽  
Author(s):  
J E Digby ◽  
J Chen ◽  
J Y Tang ◽  
H Lehnert ◽  
R N Matthews ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Human Adipose Tissue ◽  
Receptor Expression ◽  
Hormone Sensitive Lipase ◽  
Peroxisome Proliferator ◽  
Functional Responses ◽  
Orexin A ◽  
Omental Adipose Tissue

Orexin-A and orexin-B, via their receptors orexin-1 receptor (OX1R) and orexin-2 receptor (OX2R) have been shown to play a role in the regulation of feeding, body weight, and energy expenditure. Adipose tissue also contributes significantly to the maintenance of body weight by interacting with a complex array of bioactive peptides; however, there are no data as yet on the expression of orexin components in adipose tissue. We, therefore, analyzed the expression of OX1R and OX2R in human adipose tissue and determined functional responses to orexin-A and orexin-B. OX1R and OX2R mRNA expression was detected in subcutaneous (s.c.) and omental adipose tissue and in isolated adipocytes. Protein for OX1R and OX2R was also detected in whole adipose tissue sections and lysates. Treatment with orexin-A, and orexin-B (100 nM, 24 h) resulted in a significant increase in peroxisome proliferator-activated receptors γ-2 mRNA expression in s.c. adipose tissue (P < 0.05). Hormone sensitive lipase mRNA was significantly reduced in omental adipose tissue with orexin-A and orexin-B treatment (P < 0.05). Glycerol release from omental adipose tissue was also significantly reduced with orexin-A treatment (P < 0.05). These findings demonstrate for the first time the presence of functional orexin receptors in human adipose tissue and suggest a role for orexins in adipose tissue metabolism and adipogenesis.

Effects of adipokine zinc-α2-glycoprotein on adipose tissue metabolism after dexamethasone treatment

2019 ◽  
Vol 44 (1) ◽  
pp. 83-89
Author(s):  
Yu Qiao ◽  
Guoqiang Fan ◽  
Jun Guo ◽  
Shixing Gao ◽  
Ruqian Zhao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Group Analysis ◽  
Adenosine Monophosphate ◽  
Experimental Models ◽  
Hormone Sensitive Lipase ◽  
Nonesterified Fatty Acid ◽  
Plasma Nefa ◽  
Lipid Mobilization ◽  
Protein Levels

Zinc-α2-glycoprotein (ZAG) has been demonstrated to play a role in stimulating lipid mobilization under normal conditions. However, further studies are required to determine whether ZAG overexpression can alleviate the reduction in plasma lipid levels under stress conditions. In the present study, we investigated the effects of ZAG on lipometabolism in white adipose tissue (WAT) after dexamethasone (DEX) stimulation using C57BL/6 male mice as the experimental models. Transcript and protein levels of genes associated with the β-adrenoreceptor (β-AR)/cyclic adenosine monophosphate/protein kinase a (PKA) pathway, lipid mobilization, and energy metabolism were determined by quantitative real-time polymerase chain reaction and Western blotting. Plasma levels of nonesterified fatty acid (NEFA) were measured using an automatic biochemical analyzer. Results indicated that plasma NEFA levels were decreased in the DEX group, but NEFA levels were rescued by ZAG overexpression. ZAG overexpression resulted in the upregulation of β3-AR and phosphorylated PKA protein relative to those of the DEX group. Analysis of lipometabolism showed that protein levels of phosphorylated hormone-sensitive lipase was reduced upon DEX treatment but were restored by ZAG overexpression. For energy metabolism, ZAG significantly upregulated the protein expression of carnitine palmitoyltransferase1a and cytochrome c oxidase subunit 1 relative to those of the DEX group. In conclusion, ZAG could alleviate DEX-induced decrease in plasma NEFA levels and this could be associated with the promoting lipid mobilization in WAT.

scholarly journals Effects of a ketogenic diet on adipose tissue, liver, and serum biomarkers in sedentary rats and rats that exercised via resisted voluntary wheel running

2016 ◽  
Vol 311 (2) ◽  
pp. R337-R351 ◽  
Author(s):  
Angelia Maleah Holland ◽  
Wesley C. Kephart ◽  
Petey W. Mumford ◽  
Christopher Brooks Mobley ◽  
Ryan P. Lowery ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Ketogenic Diet ◽  
Body Mass ◽  
Wheel Running ◽  
Serum Insulin ◽  
Hormone Sensitive Lipase ◽  
Protein Markers ◽  
Sprague Dawley ◽  
Omental Adipose Tissue ◽  
Running Wheels

We investigated the effects of different diets on adipose tissue, liver, serum morphology, and biomarkers in rats that voluntarily exercised. Male Sprague-Dawley rats (∼9–10 wk of age) exercised with resistance-loaded voluntary running wheels (EX; wheels loaded with 20–60% body mass) or remained sedentary (SED) over 6 wk. EX and SED rats were provided isocaloric amounts of either a ketogenic diet (KD; 20.2%-10.3%-69.5% protein-carbohydrate-fat), a Western diet (WD; 15.2%-42.7–42.0%), or standard chow (SC; 24.0%-58.0%-18.0%); n = 8–10 in each diet for SED and EX rats. Following the intervention, body mass and feed efficiency were lowest in KD rats, independent of exercise ( P < 0.05). Absolute and relative (body mass-adjusted) omental adipose tissue (OMAT) masses were greatest in WD rats ( P < 0.05), and OMAT adipocyte diameters were lowest in KD-fed rats ( P < 0.05). None of the assayed OMAT or subcutaneous (SQ) protein markers were affected by the diets [total acetyl coA carboxylase (ACC), CD36, and CEBPα or phosphorylated NF-κB/p65, AMPKα, and hormone-sensitive lipase (HSL)], although EX unexpectedly altered some OMAT markers (i.e., higher ACC and phosphorylated NF-κB/p65, and lower phosphorylated AMPKα and phosphorylated HSL). Liver triglycerides were greatest in WD rats ( P < 0.05), and liver phosphorylated NF-κB/p65 was lowest in KD rats ( P < 0.05). Serum insulin, glucose, triglycerides, and total cholesterol were greater in WD and/or SC rats compared with KD rats ( P < 0.05), and serum β-hydroxybutyrate was greater in KD vs. SC rats ( P < 0.05). In conclusion, KD rats presented a healthier metabolic profile, albeit the employed exercise protocol minimally impacts any potentiating effects that KD has on fat loss.

Lipid metabolism in omental adipose tissue during operative surgery1

2005 ◽  
Vol 124 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Jaswinder Singh Samra ◽  
Paul Sved ◽  
David Sullivan ◽  
Thomas Jonathan Hugh ◽  
Ross Cyril Smith
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Omental Adipose Tissue

scholarly journals Prostaglandin F2 and EP2 Agonists Exert Different Effects on 3D 3T3-L1 Spheroids during Their Culture Phase

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1821
Author(s):  
Yosuke Ida ◽  
Masato Furuhashi ◽  
Megumi Watanabe ◽  
Araya Umetsu ◽  
Fumihito Hikage ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Mrna Expression ◽  
Three Dimensional ◽  
Two Dimensional ◽  
3D Cultures ◽  
Culture Phase ◽  
3D Spheroids

To elucidate the effects of switching a PGF2α agonist, bimatoprost acid (BIM-A), to an EP2 agonist (Omidenepag—OMD; butaprost—Buta) or reversing the switching on adipose tissue, two-dimensional (2D) and three-dimensional (3D) cultures of 3T3-L1 cells were analyzed by lipid staining and according to the mRNA expression of adipogenesis-related genes (Pparγ, Ap2, and Leptin), components of the extracellular matrix (ECM; collagen1 (Col1), Col4, Col6, and fibronectin (Fn)), and the sizes and stiffness of the 3D spheroids. Switching from BIM-A to EP2 agonists caused (1) suppression of lipid staining and downregulation of most adipogenesis-related genes, (2) smaller and stiffer 3D spheroids, and (3) upregulation of Col1 and Fn, downregulation of Col4 (2D), or up-regulation of all ECM genes (3D, BIM-A to OMD), as well as downregulation of Col6 (3D, BIM-A to Buta). In contrast, reversing the switching resulted in (1) an enhancement in lipid staining (2D) and a significant upregulation of adipogenesis-related genes (2D, 3D Buta to BIM-A), (2) larger and slightly stiffer 3D spheroids, and (3) upregulation of Col1 and Fn (2D). These collective findings indicate that the switching orders of BIM-A and EP2 agonists have a significant effect on lipid metabolism, ECM expression, and the physical stiffness of 3T3-L1 cells.

scholarly journals Genistein Induces Adipogenic and Autophagic Effects in Rainbow Trout (Oncorhynchus mykiss) Adipose Tissue: In Vitro and In Vivo Models

2020 ◽  
Vol 21 (16) ◽  
pp. 5884
Author(s):  
Sara Balbuena-Pecino ◽  
Esmail Lutfi ◽  
Natàlia Riera-Heredia ◽  
Esther Gasch-Navalón ◽  
Emilio J. Vélez ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Rainbow Trout ◽  
Lipid Metabolism ◽  
Oncorhynchus Mykiss ◽  
Fatty Acid Synthase ◽  
Hormone Sensitive Lipase ◽  
In Vivo Models ◽  
Rainbow Trout Oncorhynchus Mykiss

Soybeans are one of the most used alternative dietary ingredients in aquafeeds. However, they contain phytoestrogens like genistein (GE), which can have an impact on fish metabolism and health. This study aimed to investigate the in vitro and in vivo effects of GE on lipid metabolism, apoptosis, and autophagy in rainbow trout (Oncorhynchus mykiss). Primary cultured preadipocytes were incubated with GE at different concentrations, 10 or 100 μM, and 1 μM 17β-estradiol (E2). Furthermore, juveniles received an intraperitoneal injection of GE at 5 or 50 µg/g body weight, or E2 at 5 µg/g. In vitro, GE 100 μM increased lipid accumulation and reduced cell viability, apparently involving an autophagic process, indicated by the higher LC3-II protein levels, and higher lc3b and cathepsin d transcript levels achieved after GE 10 μM. In vivo, GE 50 µg/g upregulated the gene expression of fatty acid synthase (fas) and glyceraldehyde-3-phosphate dehydrogenase in adipose tissue, suggesting enhanced lipogenesis, whereas it increased hormone-sensitive lipase in liver, indicating a lipolytic response. Besides, autophagy-related genes increased in the tissues analyzed mainly after GE 50 µg/g treatment. Overall, these findings suggest that an elevated GE administration could lead to impaired adipocyte viability and lipid metabolism dysregulation in rainbow trout.

Regulation of lipid metabolism in adipose tissue during early starvation

1996 ◽  
Vol 271 (3) ◽  
pp. E541-E546 ◽  
Author(s):  
J. S. Samra ◽  
M. L. Clark ◽  
S. M. Humphreys ◽  
I. A. Macdonald ◽  
K. N. Frayn
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Strong Relationship ◽  
Venous Drainage ◽  
Hormone Sensitive Lipase ◽  
Nonesterified Fatty Acid ◽  
Plasma Insulin Concentration ◽  
Relative Contribution ◽  
Hormone Sensitive ◽  
Subcutaneous Adipose

We studied changes in lipid metabolism in adipose tissue in 24 healthy adults during early starvation (14-20 h) by cannulating the venous drainage of the subcutaneous adipose tissue of the anterior abdominal wall. Net nonesterified fatty acid (NEFA) efflux from adipose tissue increased steadily from 1,790 +/- 300 to 2,360 +/- 290 nmol.100 g-1.min-1 (P = 0.03), due to increasing transcapillary efflux of NEFA (release from adipocytes; P < 0.01). The reesterification rate after an overnight fast was close to zero; thus, reduction in the rate of reesterification played no part in the increased transcapillary efflux of NEFA. One-quarter of the net efflux of NEFA after an overnight fast arose from the action of lipoprotein lipase (LPL), although this relative contribution decreased during the study (P < 0.02). The increased transcapillary efflux of NEFA reflected a significant increase in the rate of action of hormone-sensitive lipase (HSL; P = 0.03). There was a strong relationship between mean arterial NEFA concentration and net NEFA release from adipose tissue (P < 0.001), implying that the particular depot studied reflects the behavior of adipose tissue as a whole. Thus the increasing efflux of NEFA from adipose tissue observed during early starvation is due to an increased rate of action of HSL, which may in turn be regulated by a fall in the plasma insulin concentration.

scholarly journals The Effects of New Selective PPARα Agonist CP775146 on Systematic Lipid Metabolism in Obese Mice and Its Potential Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shengjie Tang ◽  
Fang Wu ◽  
Xihua Lin ◽  
Weiwei Gui ◽  
Fenping Zheng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Uncoupling Protein ◽  
Density Lipoprotein ◽  
Hormone Sensitive Lipase ◽  
Lipoprotein Cholesterol ◽  
Obese Mice ◽  
Liver Fatty Acid ◽  
Expression Of Genes

Purpose. Peroxisome proliferator-activated receptor α (PPARα) plays a crucial role in the control of lipid homeostasis. Here, we investigated the effects of CP775146, a new selective PPARα agonist, on lipid metabolism in diet-induced obese mice and its possible mechanism. Methods. C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity and then received CP775146 via intraperitoneal injection for 3 days. The content/morphology of the liver, serum lipid, and liver function was measured. The expression of genes related to lipolysis and synthesis in liver was detected by quantitative real-time PCR (qRT-PCR). Results. The safe dose of CP775146 was <0.3 mg/kg. CP775146 reduced the serum levels of liver enzymes, such as alanine aminotransferase (ALT) and glutamic-oxaloacetic transaminase (AST) and lipid metabolism-related biomarkers, including triglycerides (TGs) and low-density lipoprotein cholesterol (LDL-c), non-high-density lipoprotein cholesterol (non-HDL-c), and hepatic TG content, at a dosage of 0.1 mg/kg. HFD-induced pathological liver changes improved after CP775146 treatment. The expression of genes involved in liver fatty acid oxidation (acyl-coenzyme A dehydrogenase, long chain (Acadl), acyl-CoA oxidase 1 (Acox-1), carnitine palmitoyltransferase-1 (CPT-1), and enoyl-CoA, hydratase/3-hydroxyacyl CoA dehydrogenase (Ehhadh)) was upregulated in CP775146-treated mice. Furthermore, CP775146 induced the expression of thermogenesis genes (cell death-inducing DFFA-like effector a (Cidea), uncoupling protein 1 (Ucp1)) and lipolysis genes (hormone-sensitive lipase (Hsl), adipose tissue triglyceride lipase (Atgl)) in epididymal white adipose tissue (eWAT), activating browning and thermogenesis. Conclusion. CP775146 efficiently alleviates obesity-induced liver damage, prevents lipid accumulation by activating the liver fatty acid β-oxidation pathway, and regulates the expression of genes that control brown fat-like pathway in eWAT.

scholarly journals The effect of placental restriction on insulin signaling and lipogenic pathways in omental adipose tissue in the postnatal lamb

2013 ◽  
Vol 4 (5) ◽  
pp. 421-429 ◽  
Author(s):  
S. Lie ◽  
J. A. Duffield ◽  
I. C. McMillen ◽  
J. L. Morrison ◽  
S. E. Ozanne ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Insulin Signaling ◽  
Visceral Obesity ◽  
Signaling Molecules ◽  
Protein Abundance ◽  
Adipose Depot ◽  
Omental Adipose Tissue ◽  
Lipogenic Genes ◽  
Neonatal Lambs

Intrauterine growth restriction (IUGR) followed by accelerated growth after birth is associated with an increased risk of abdominal (visceral) obesity and insulin resistance in adult life. The aim of the present study was to determine the impact of IUGR on mRNA expression and protein abundance of insulin signaling molecules in one of the major visceral fat depots, the omental adipose depot. IUGR was induced by placental restriction, and samples of omental adipose tissue were collected from IUGR (n = 9, 5 males, 4 females) and Control (n = 14, 8 males, 6 females) neonatal lambs at 21 days of age. The mRNA expression of the insulin signaling molecules, AMP-kinase (AMPK) and adipogenic/lipogenic genes was determined by qRT-PCR, and protein abundance by Western Blotting. AMPKα2 mRNA expression was increased in male IUGR lambs (0.015 ± 0.002 v. 0.0075 ± 0.0009, P < 0.001). The proportion of the AMPK pool that was phosphorylated (%P-AMPK) was lower in IUGR lambs compared with Controls independent of sex (39 ± 9% v. 100 ± 18%, P < 0.001). The mRNA expression and protein abundance of insulin signaling proteins and adipogenic/lipogenic genes was not different between groups. Thus, IUGR is associated with sex-specific alterations in the mRNA expression of AMPKα2 and a reduction in the percentage of the total AMPK pool that is phosphorylated in the omental adipose tissue of neonatal lambs, before the onset of visceral obesity. These molecular changes would be expected to promote lipid accumulation in the omental adipose depot and may therefore contribute to the onset of visceral adiposity in IUGR animals later in life.

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