scholarly journals Skeletal Muscle Lipidomics as a New Tool to Determine Altered Lipid Homeostasis in Fish Exposed to Urban and Industrial Wastewaters

2019 ◽  
Vol 53 (14) ◽  
pp. 8416-8425 ◽  
Author(s):  
Anna Marqueño ◽  
Maria Blanco ◽  
Alberto Maceda-Veiga ◽  
Cinta Porte
Keyword(s):  
Skeletal Muscle ◽  
Lipid Homeostasis ◽  
Industrial Wastewaters ◽  
Altered Lipid

scholarly journals The Effect of Combined Diet Containing n-3 Polyunsaturated Fatty Acids and Silymarin on Metabolic Syndrome in Rats

2019 ◽  
pp. S39-S50
Author(s):  
M. PORUBA ◽  
P. ANZENBACHER ◽  
Z. RACOVA ◽  
O. OLIYARNYK ◽  
M. HÜTTL ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Metabolic Disorders ◽  
Male Rats ◽  
Lipid Homeostasis ◽  
Metabolic Disturbances ◽  
Serum Triglycerides ◽  
Esterified Fatty Acids

The risk of development of metabolic syndrome can be increased by hypertriglyceridemia. A search for effective therapy is a subject of considerable attention. Therefore, our hypothesis is that the fish oil (containing polyunsaturated fatty acids; n-3 PUFA) in a combination with silymarin can more effectively protect against hypertriglyceridemia-induced metabolic disturbances. The study was conducted using a unique non-obese strain of rats with hereditary hypertriglyceridemia an accepted model of metabolic syndrome. Adult male rats were treated with n-3 PUFA (300 mg/kg/day) without or with 1 % micronized silymarin in a diet for 4 weeks. The treatment with the diet containing n-3 PUFA and silymarin significantly reduced concentrations of serum triglycerides (-45 %), total cholesterol (-18 %), non-esterified fatty acids (-33 %), and ectopic lipid accumulation in skeletal muscle (-35 %) compared to controls. In addition, an increase in Abcg5 and Abcg8 mRNA expression (as genes affecting lipid homeostasis) as well as in protein content of ABCG5 (+78 %) and ABCG8 (+232 %) transporters have been determined in the liver of treated rats. Our findings suggest that this combined diet could be used in the prevention of hypertriglyceridemia-induced metabolic disorders.

scholarly journals Peroxisome Proliferator-Activated Receptor Delta: A Conserved Director of Lipid Homeostasis through Regulation of the Oxidative Capacity of Muscle

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Pieter de Lange ◽  
Assunta Lombardi ◽  
Elena Silvestri ◽  
Fernando Goglia ◽  
Antonia Lanni ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Oxidative Capacity ◽  
Whole Body ◽  
Lipid Homeostasis ◽  
Peroxisome Proliferator ◽  
Transcriptional Program ◽  
Peroxisome Proliferator Activated Receptor ◽  
Peroxisome Proliferator Activated Receptors ◽  
Metabolic Action

The peroxisome proliferator-activated receptors (PPARs), which are ligand-inducible transcription factors expressed in a variety of tissues, have been shown to perform key roles in lipid homeostasis. In physiological situations such as fasting and physical exercise, one PPAR subtype, PPARδ, triggers a transcriptional program in skeletal muscle leading to a switch in fuel usage from glucose/fatty acids to solely fatty acids, thereby drastically increasing its oxidative capacity. The metabolic action of PPARδ has also been verified in humans. In addition, it has become clear that the action of PPARδ is not restricted to skeletal muscle. Indeed, PPARδ has been shown to play a crucial role in whole-body lipid homeostasis as well as in insulin sensitivity, and it is active not only in skeletal muscle (as an activator of fat burning) but also in the liver (where it can activate glycolysis/lipogenesis, with the produced fat being oxidized in muscle) and in the adipose tissue (by incrementing lipolysis). The main aim of this review is to highlight the central role for activated PPARδ in the reversal of any tendency toward the development of insulin resistance.

scholarly journals Altered Lipid Homeostasis in Sertoli Cells Stressed by Mild Hyperthermia

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e91127 ◽  
Author(s):  
Ana S. Vallés ◽  
Marta I. Aveldaño ◽  
Natalia E. Furland
Keyword(s):  
Sertoli Cells ◽  
Lipid Homeostasis ◽  
Mild Hyperthermia ◽  
Altered Lipid

scholarly journals Altered lipid homeostasis in Drosophila InsP3 receptor mutants leads to obesity and hyperphagia

2013 ◽  
Vol 6 (3) ◽  
pp. 734-744 ◽  
Author(s):  
M. Subramanian ◽  
S. K. Metya ◽  
S. Sadaf ◽  
S. Kumar ◽  
D. Schwudke ◽  
...  
Keyword(s):  
Lipid Homeostasis ◽  
Altered Lipid ◽  
Insp3 Receptor

scholarly journals Myonectin (CTRP15), a Novel Myokine That Links Skeletal Muscle to Systemic Lipid Homeostasis

2012 ◽  
Vol 287 (15) ◽  
pp. 11968-11980 ◽  
Author(s):  
Marcus M. Seldin ◽  
Jonathan M. Peterson ◽  
Mardi S. Byerly ◽  
Zhikui Wei ◽  
G. William Wong
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Energy State ◽  
Voluntary Exercise ◽  
Whole Body ◽  
Lipid Homeostasis ◽  
Acid Uptake ◽  
Related Protein ◽  
Circulating Levels

Skeletal muscle plays important roles in whole-body glucose and fatty acid metabolism. However, muscle also secretes cytokines and growth factors (collectively termed myokines) that can potentially act in an autocrine, a paracrine, and/or an endocrine manner to modulate metabolic, inflammatory, and other processes. Here, we report the identification and characterization of myonectin, a novel myokine belonging to the C1q/TNF-related protein (CTRP) family. Myonectin transcript was highly induced in differentiated myotubes and predominantly expressed by skeletal muscle. Circulating levels of myonectin were tightly regulated by the metabolic state; fasting suppressed, but refeeding dramatically increased, its mRNA and serum levels. Although mRNA and circulating levels of myonectin were reduced in a diet-induced obese state, voluntary exercise increased its expression and circulating levels. Accordingly, myonectin transcript was up-regulated by compounds (forskolin, epinephrine, ionomycin) that raise cellular cAMP or calcium levels. In vitro, secreted myonectin forms disulfide-linked oligomers, and when co-expressed, forms heteromeric complexes with other members of the C1q/TNF-related protein family. In mice, recombinant myonectin administration reduced circulating levels of free fatty acids without altering adipose tissue lipolysis. Consistent with this, myonectin promoted fatty acid uptake in cultured adipocytes and hepatocytes, in part by up-regulating the expression of genes (CD36, FATP1, Fabp1, and Fabp4) that promote lipid uptake. Collectively, these results suggest that myonectin links skeletal muscle to lipid homeostasis in liver and adipose tissue in response to alterations in energy state, revealing a novel myonectin-mediated metabolic circuit.

scholarly journals Targeting RalGAPα1 in skeletal muscle to simultaneously improve postprandial glucose and lipid control

2019 ◽  
Vol 5 (4) ◽  
pp. eaav4116
Author(s):  
Qiaoli Chen ◽  
Ping Rong ◽  
Sangsang Zhu ◽  
Xinyu Yang ◽  
Qian Ouyang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transporter ◽  
Postprandial Glucose ◽  
Lipid Homeostasis ◽  
Dual Purpose ◽  
Diet Induced Obesity ◽  
Glucose And Lipid Homeostasis ◽  
Lipid Control ◽  
Glucose Transporter Glut4 ◽  
Muscle Insulin Action

How insulin stimulates postprandial uptake of glucose and long-chain fatty acids (LCFAs) into skeletal muscle and the mechanisms by which these events are dampened in diet-induced obesity are incompletely understood. Here, we show that RalGAPα1 is a critical regulator of muscle insulin action and governs both glucose and lipid homeostasis. A high-fat diet increased RalGAPα1 protein but decreased its insulin-responsive Thr735-phosphorylation in skeletal muscle. A RalGAPα1Thr735Ala mutation impaired insulin-stimulated muscle assimilation of glucose and LCFAs and caused metabolic syndrome in mice. In contrast, skeletal muscle–specific deletion of RalGAPα1 improved postprandial glucose and lipid control. Mechanistically, these mutations of RalGAPα1 affected translocation of insulin-responsive glucose transporter GLUT4 and fatty acid translocase CD36 via RalA to affect glucose and lipid homeostasis. These data indicated RalGAPα1 as a dual-purpose target, for which we developed a peptide-blockade for improving muscle insulin sensitivity. Our findings have implications for drug discovery to combat metabolic disorders.

Sign in / Sign up

Export Citation Format

Share Document