scholarly journals THE ROLE OF MYOKINES INTERSTITIAL INTERACTION AND REGULATION OF METABOLISM: A REVIEW OF LITERATURE

2016 ◽  
Vol 19 (1) ◽  
pp. 28-34
Author(s):  
T T Tsoriev ◽  
Zh E White ◽  
L Ya Rozhinskaya
Keyword(s):  
Skeletal Muscles ◽  
Metabolic Disorders ◽  
Visceral Obesity ◽  
Signal Pathways ◽  
Review Of Literature ◽  
Glucose And Lipid Metabolism ◽  
Regulation Of Metabolism ◽  
Skin Mucosa

Myokines are hormone-like acting molecules produced in skeletal muscles during and immediately after exercise. They affect both paracrine (inside the muscles themselves) and endocrine manner (in adipose tissue, liver, endothelium, skin, mucosa etc.) implementing different effects on target tissues, mainly through regulation of metabolic processes (such as glucose and lipid metabolism, growth and division of neurons and endothelial cells and others). The examination of myokines is of great interest for researchers of different medicine departments, particularly for endocrinologists, because of myokines’ involvement in pathogenesis of abdominal and visceral obesity, diabetes mellitus type 2 and cardiovascular diseases that are all the components of metabolic syndrome. The most important issue for clinicians is a possibility of future therapeutic implication of the myokine’s signal pathways in treatment of widespread metabolic disorders.

scholarly journals ANGPTL8 in metabolic homeostasis: more friend than foe?

Open Biology ◽  
2021 ◽  
Vol 11 (9) ◽  
Author(s):  
Chang Guo ◽  
Chenxi Wang ◽  
Xia Deng ◽  
Jianqiang He ◽  
Ling Yang ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Hepatic Glucose Production ◽  
Physiological Role ◽  
Glucose Production ◽  
Peripheral Tissues ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Glucose

ANGPTL8 is an important cytokine, which is significantly increased in type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. Many studies have shown that ANGPTL8 can be used as a bio-marker of these metabolic disorders related diseases, and the baseline ANGPTL8 level has also been found to be positively correlated with retinopathy and all-cause mortality in patients with T2DM. This may be related to the inhibition of lipoprotein lipase activity and the reduction of circulating triglyceride (TG) clearance by ANGPTL8. Consistently, inhibition of ANGPTL8 seems to prevent or improve atherosclerosis. However, it is puzzling that ANGPTL8 seems to have a directing function for TG uptake in peripheral tissues; that is, ANGPTL8 specifically enhances the reserve and buffering function of white adipose tissue, which may alleviate the ectopic lipid accumulation to a certain extent. Furthermore, ANGPTL8 can improve insulin sensitivity and inhibit hepatic glucose production. These contradictory results lead to different opinions on the role of ANGPTL8 in metabolic disorders. In this paper, the correlation between ANGPTL8 and metabolic diseases, the regulation of ANGPTL8 and the physiological role of ANGPTL8 in the process of glucose and lipid metabolism were summarized, and the physiological/pathological significance of ANGPTL8 in the process of metabolic disorder was discussed.

scholarly journals The NLRP3 Inflammasome as a Novel Player of the Intercellular Crosstalk in Metabolic Disorders

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Elisa Benetti ◽  
Fausto Chiazza ◽  
Nimesh S. A. Patel ◽  
Massimo Collino
Keyword(s):  
Chronic Inflammation ◽  
Nlrp3 Inflammasome ◽  
Metabolic Disorders ◽  
Inflammasome Activation ◽  
Nucleotide Binding Domain ◽  
Metabolic Inflammation ◽  
Nlrp3 Inflammasome Activation ◽  
Leucine Rich Repeat Protein

The combination of obesity and type 2 diabetes is a serious health problem, which is projected to afflict 300 million people worldwide by 2020. Both clinical and translational laboratory studies have demonstrated that chronic inflammation is associated with obesity and obesity-related conditions such as insulin resistance. However, the precise etiopathogenetic mechanisms linking obesity to diabetes remain to be elucidated, and the pathways that mediate this phenomenon are not fully characterized. One of the most recently identified signaling pathways, whose activation seems to affect many metabolic disorders, is the “inflammasome,” a multiprotein complex composed of NLRP3 (nucleotide-binding domain and leucine-rich repeat protein 3), ASC (apoptosis-associated speck-like protein containing a CARD), and procaspase-1. NLRP3 inflammasome activation leads to the processing and secretion of the proinflammatory cytokines interleukin- (IL-) 1βand IL-18. The goal of this paper is to review new insights on the effects of the NLRP3 inflammasome activation in the complex mechanisms of crosstalk between different organs, for a better understanding of the role of chronic inflammation in metabolic disease pathogenesis. We will provide here a perspective on the current research on NLRP3 inflammasome, which may represent an innovative therapeutic target to reverse the detrimental metabolic consequences of the metabolic inflammation.

scholarly journals Association Study of Candidate Gene Uncoupling Protein 2 (UCP2) with Type 2 Diabetes Mellitus in the Different Population Groups of Jammu Region

2019 ◽  
Vol 16 (2) ◽  
pp. 351-357
Author(s):  
Sunil Raina ◽  
Roopali Fotra
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Disorders ◽  
Uncoupling Protein ◽  
Molecular Genetic ◽  
Promoter Polymorphism ◽  
Uncoupling Protein 2 ◽  
Population Groups ◽  
Allelic Odds Ratio

Diabetes Mellitus is a group of metabolic disorders characterized by hyperglycaemic resulting from the defects of insulin secretion, insulin action or both. The present study was conducted in order to know the molecular genetic cause of the T2DM patients belonging to the Jammu region of J&K State. Many genes have been known to be linked with the onset and progression of the T2DM therefore the present data represents the role of one of the genes Uncoupling protein 2 (UCP2) known to be strongly associated with T2DM was selected. A total of 250 confirmed cases & controls samples belonging to four population groups (Hindu, Muslim, Sikh & Christians) of Jammu region were also screened for UCP2 -866G/A promoter polymorphism (rs659366). The allelic odds ratio (OR) as observed for UCP2 -866G/A polymorphism in the four population groups showed significant association with Muslim & Sikh population groups. The study undertaken supports the findings of the previous investigations and thus is an addition to the existing literatute in support of UCP2 and T2DM.

scholarly journals A Transcriptomic and Proteomic Atlas of Obesity and Type 2 Diabetes in Cynomolgus Monkeys

2021 ◽  
Author(s):  
Xianglong Zhang ◽  
Ying Lei ◽  
Oliver Homann ◽  
Marina Stolina ◽  
Songli Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immune Response ◽  
Nonhuman Primate ◽  
Metabolic Disorders ◽  
Healthy Controls ◽  
Adipose Tissues ◽  
Cynomolgus Monkeys ◽  
Single Cell Rna Sequencing

Obesity and type 2 diabetes (T2D) remain major global healthcare challenges and developing therapeutics necessitate using nonhuman primate models. Here, we present transcriptomic and proteomic analyses of all the major organs of cynomolgus monkeys with spontaneous obesity or T2D in comparison to healthy controls. Molecular changes occur predominantly in the adipose tissues of individuals with obesity, while extensive expression perturbations among T2D individuals are observed in many tissues, such as the liver, kidney, brain, and heart. Immune response-related pathways are upregulated in obesity and T2D, whereas metabolism and mitochondrial pathways are downregulated. Incorporating human single-cell RNA sequencing findings corroborates the role of macrophages and monocytes in obesity. Moreover, we highlight some potential therapeutic targets including SLC2A1 and PCSK1 in obesity as well as SLC30A8 and SLC2A2 in T2D. Our findings provide insights into tissue-specific molecular foundations of obesity and T2D and reveal the mechanistic links between these two metabolic disorders.

The harp seal, Pagophilus groenlandicus (Erxleben, 1777). VII. A histophysiological study of certain skeletal muscles

1971 ◽  
Vol 49 (1) ◽  
pp. 25-30 ◽  
Author(s):  
J. C. George ◽  
N. V. Vallyathan ◽  
K. Ronald
Keyword(s):  
Skeletal Muscles ◽  
Biochemical Properties ◽  
Histochemical Demonstration ◽  
Harp Seal ◽  
Activity Levels ◽  
Sodium Pentobarbital ◽  
Pagophilus Groenlandicus

A quantitative and histochemical study of Ms. pectoralis, gluteus, psoas, diaphragma (dorsal, lateral, and ventral parts separately) of the harp seal was carried out. Myoglobin and iron contents of all the muscles were high, highest being of M. psoas. Fat and glycogen were low in all muscles. The low glycogen value was possibly due to rapid glycolysis during struggle in capture and while the animal was under an overdose of sodium pentobarbital that was administered for killing it. Phosphorylase and succinate dehydrogenase (SDH) activity levels were also low. Lipase (tributyrinase) activity was high, that of M. diaphragma being higher than the other muscles studied. The histochemical investigation revealed some of the morphological and biochemical properties of the component fibers. Two types of fiber, the red (type 1) and white (type 2), comparable to those of other skeletal muscles were distinguished in all muscles except in the case of M. pectoralis where an intermediate type was also seen in sections treated for the histochemical demonstration of SDH activity.The low levels of fat and SDH in the muscles indicate that fat is not a favored metabolite for muscular energy. The significance of the high lipase (tributyrinase) activity is doubtful. It is suggested that the role of this enzyme is to clear the fat so as to prevent the accumulation of fat in the muscles which are, by and large, geared for a glycolytic metabolism as an adaptation for the animal's diving habit. The high myoglobin content of the muscles, however, should provide the oxygen necessary for the oxidation of glucose during the initial part of the dive.

scholarly journals Potential Roles of Adipocyte Extracellular Vesicle–Derived miRNAs in Obesity-Mediated Insulin Resistance

2020 ◽  
Author(s):  
Yujeong Kim ◽  
Ok-Kyung Kim
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Metabolic Disorders ◽  
Extracellular Vesicle ◽  
Extracellular Mirnas

ABSTRACT Recently, extracellular microRNAs (miRNAs) from adipose tissue have been shown to be involved in the development of insulin resistance. Here, we summarize several mechanisms explaining the pathogenesis of obesity-induced insulin resistance and associated changes in the expression of obesity-associated extracellular miRNAs. We discuss how miRNAs, particularly miR-27a, miR-34a, miR-141-3p, miR-155, miR210, and miR-222, in extracellular vesicles secreted from the adipose tissue can affect the insulin signaling pathway in metabolic tissue. Understanding the role of these miRNAs will further support the development of therapeutics for obesity and metabolic disorders such as type 2 diabetes.

Emerging role of nutrition and the non-coding landscape in type 2 diabetes mellitus: A review of literature

Gene ◽  
2018 ◽  
Vol 675 ◽  
pp. 54-61 ◽  
Author(s):  
Marwa Matboli ◽  
Ayman Shafei ◽  
Mahmoud Ali ◽  
Kamal M. Kamal ◽  
Mahmoud Noah ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Review Of Literature

scholarly journals The Liver under the Spotlight: Bile Acids and Oxysterols as Pivotal Actors Controlling Metabolism

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 400
Author(s):  
Charlotte Lefort ◽  
Patrice D. Cani
Keyword(s):  
Bile Acids ◽  
Metabolic Disorders ◽  
Energy Homeostasis ◽  
Inflammatory Diseases ◽  
Attractive Potential ◽  
Bioactive Lipids ◽  
Glucose And Lipid Metabolism ◽  
Long Time ◽  
New Treatments

Among the myriad of molecules produced by the liver, both bile acids and their precursors, the oxysterols are becoming pivotal bioactive lipids which have been underestimated for a long time. Their actions are ranging from regulation of energy homeostasis (i.e., glucose and lipid metabolism) to inflammation and immunity, thereby opening the avenue to new treatments to tackle metabolic disorders associated with obesity (e.g., type 2 diabetes and hepatic steatosis) and inflammatory diseases. Here, we review the biosynthesis of these endocrine factors including their interconnection with the gut microbiota and their impact on host homeostasis as well as their attractive potential for the development of therapeutic strategies for metabolic disorders.

scholarly journals The role of LEPR, PPARG and PPARGC1A genes polymorphisms in the development of metabolic disorders in patients with vibration diseases

2021 ◽  
Vol 100 (7) ◽  
pp. 711-716
Author(s):  
Liudmila B. Masnavieva ◽  
Nadezhda P. Chistova ◽  
Olga V. Naumova ◽  
Irina V. Kudaeva
Keyword(s):  
Metabolic Syndrome ◽  
Metabolic Disorders ◽  
Polymorphic Locus ◽  
Protective Role ◽  
Local Vibration ◽  
Lepr Gene ◽  
Male Patients ◽  
Combined Impact

Introduction. Patients with vibration disease (VD) often have obesity and metabolic syndrome (MS), which increase the risk of developing type 2 diabetes, hypertension, and other conditions predisposing to a decrease in the quality and longevity of life. Genetic predisposition, overnutrition, environmental factors, including industrial ones, and others are factors influencing the formation of MS. The aim of the study is to identify associations between polymorphisms of the LEPR, PPARG and PPARGC1A genes, metabolic syndrome and obesity in VD patients caused by exposure to local vibration and the combined effects of local and general vibration. Material and methods. We examined 248 VD male patients exposed to local vibration and the combined impact of the local and general vibration. We have identified a subgroup of MS and obesity cases. The distribution of genotypes of the LEPR, PPARG and PPARGC1A genes in groups was studied. Results. In the group of VD and MS patients exposed to the combined effect of local and general vibration, the Gln/Gln genotype of the Arg223Gln polymorphic locus of the LEPR gene was less common, and the Arg / Gln genotype in MS cases was detected more often than in patients without it. Among patients with VD caused by exposure to local vibration with a waist circumference of more than 102 cm, the Gly / Ser genotype of the Gly482Ser polymorphism of the PPARGC1A gene was more common than among those with lower values of this indicator. Conclusion. In patients with VD caused by combined exposure to local and general vibration, the Gln/Gln genotype carrier of the Arg223Gln polymorphism of the LEPR gene may play a protective role in the formation of MS. Among individuals with VD caused by exposure to local vibration, carriers of the heterozygous genotype of the Gly482Ser polymorphism of the PPARGC1A gene may have a predisposition to the development of obesity. The obtained results are preliminary and require further research.

scholarly journals Metformin Stimulates FGF21 Expression in Primary Hepatocytes

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Eva B. Nygaard ◽  
Sara G. Vienberg ◽  
Cathrine Ørskov ◽  
Harald S. Hansen ◽  
Birgitte Andersen
Keyword(s):  
Human Hepatocytes ◽  
Fibroblast Growth Factor 21 ◽  
Potent Inducer ◽  
Glucose And Lipid Metabolism ◽  
Compound C ◽  
Mrna And Protein Expression ◽  
Dose Dependent Increase ◽  
Fgf21 Expression

Fibroblast growth factor 21 (FGF21) is a novel metabolic regulator of glucose and lipid metabolism; however, the exact mechanism of action and regulation of FGF21 is not fully understood. Metabolic status plays an important role in the regulation of FGF21, and we therefore examined whether metformin, an indirect AMPK-activator, regulates FGF21 expression in hepatocytes. FGF21 mRNA and protein expression were determined after incubation of primary cultured rat and human hepatocytes with metformin for 24 hours. To study the role of AMPK in the putative regulation of FGF21, hepatocytes were incubated with Compound C (an AMPK inhibitor) in the presence of metformin. A strong dose-dependent increase in FGF21 expression was observed in both rat and human hepatocytes treated with metformin. This effect was blocked by addition of the AMPK-inhibitor Compound C. The study shows that metformin is a potent inducer of hepatic FGF21 expression and that the effect of metformin seems to be mediated through AMPK activation. As FGF21 therapy normalizes blood glucose in animal models of type 2 diabetes, the induction of hepatic FGF21 by metformin might play an important role in metformin’s antidiabetic effect.

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