scholarly journals Melanocortin crosstalk with adipose functions: ACTH directly induces insulin resistance, promotes a pro-inflammatory adipokine profile and stimulates UCP-1 in adipocytes

2007 ◽  
Vol 196 (3) ◽  
pp. 465-472 ◽  
Author(s):  
K Alexander H Iwen ◽  
Oezge Senyaman ◽  
Arne Schwartz ◽  
Maren Drenckhan ◽  
Britta Meier ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Uncoupling Protein ◽  
Mitogen Activated Protein Kinase ◽  
Stress Axis ◽  
Mrna Levels ◽  
Acth Stimulation ◽  
Brown Adipocytes ◽  
The Metabolic Syndrome ◽  
Acth Treatment

The melanocortin (MC) system is a pivotal component of the hypothalamo-pituitary–adrenal (HPA) stress axis and plays an important role in the pathogenesis of obesity and the metabolic syndrome. Adipose dysfunction is implicated in the pathogenesis of these disorders. We investigated direct ACTH effects on adipose functions in immortalised murine white and brown adipocytes. MC receptor types 2 and 5 were expressed at the mRNA and protein levels and were strongly up-regulated during differentiation. Chronic ACTH stimulation did not affect adipogenesis. Insulin-induced glucose uptake in white adipocytes was acutely and transiently reduced by 45% upon ACTH treatment. Visfatin and adiponectin gene expression was reduced by about 50% in response to ACTH, while interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) mRNA levels were acutely up-regulated by 2100 and 60% respectively. Moreover, IL-6 secretion was increased by 1450% within 4 h of ACTH treatment. In brown adipocytes, stimulation with ACTH caused a 690% increase in uncoupling protein (UCP)-1 mRNA levels within 8 h, followed by a 470% increase in UCP-1 protein concentrations after 24 h. Consistently, p38 mitogen-activated protein kinase (MAPK) phosphorylation was acutely increased by 1800% in response to ACTH stimulation, and selective inhibition of p38 MAPK abolished the ACTH-mediated UCP-1 protein increase. Taken together, ACTH acutely promotes an insulin-resistant, pro-inflammatory state and transiently enhances energy combustion. In conditions characterised by a dysregulation of the HPA stress axis such as the metabolic syndrome, direct MC interaction with adipocytes may contribute to dysregulated energy balance, insulin resistance and cardiometabolic complications.

Metabolic Syndrome During Menopause

2019 ◽  
Vol 17 (6) ◽  
pp. 595-603 ◽  
Author(s):  
Sezcan Mumusoglu ◽  
Bulent Okan Yildiz
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Central Obesity ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Natural Menopause ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Aging Women

The metabolic syndrome (MetS) comprises individual components including central obesity, insulin resistance, dyslipidaemia and hypertension and it is associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The menopause per se increases the incidence of MetS in aging women. The effect(s) of menopause on individual components of MetS include: i) increasing central obesity with changes in the fat tissue distribution, ii) potential increase in insulin resistance, iii) changes in serum lipid concentrations, which seem to be associated with increasing weight rather than menopause itself, and, iv) an association between menopause and hypertension, although available data are inconclusive. With regard to the consequences of MetS during menopause, there is no consistent data supporting a causal relationship between menopause and CVD. However, concomitant MetS during menopause appears to increase the risk of CVD. Furthermore, despite the data supporting the association between early menopause and increased risk of T2DM, the association between natural menopause itself and risk of T2DM is not evident. However, the presence and the severity of MetS appears to be associated with an increased risk of T2DM. Although the mechanism is not clear, surgical menopause is strongly linked with a higher incidence of MetS. Interestingly, women with polycystic ovary syndrome (PCOS) have an increased risk of MetS during their reproductive years; however, with menopausal transition, the risk of MetS becomes similar to that of non-PCOS women.

C-Peptide and its Correlation to Parameters of Insulin Resistance in the Metabolic Syndrome

2011 ◽  
Vol 10 (8) ◽  
pp. 921-927 ◽  
Author(s):  
Shaheena Banu ◽  
Nasimudeen R. Jabir ◽  
C. N. Manjunath ◽  
Shazi Shakil ◽  
Mohammad A. Kamal
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
C Peptide ◽  
The Metabolic Syndrome

scholarly journals Risk Factors of Metabolic Syndrome among Polish Nurses

Metabolites ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 267
Author(s):  
Anna Bartosiewicz ◽  
Edyta Łuszczki ◽  
Małgorzata Nagórska ◽  
Łukasz Oleksy ◽  
Artur Stolarczyk ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Weight Control ◽  
Professional Group ◽  
Overweight And Obesity ◽  
World Health ◽  
Dietary Recommendations ◽  
Obesity Class ◽  
The Metabolic Syndrome ◽  
The World

The metabolic syndrome, also known as syndrome X or the insulin resistance, is defined by the World Health Organization as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Both all over the world and in Poland, there is a shortage of nurses; most of those employed are in the pre-retirement age. However, the requirements in this profession and the patient’s right to care at the highest level remain unchanged and do not take into account the poor condition or age of working nurses, so special attention should be paid to the state of health in this professional group. There is an emphasis on the importance of the adopted attitude toward health and the resulting behaviors, such as regular weight control, following dietary recommendations, regular physical activity and participation in preventive examinations. The aim of the study was to assess the frequency of the occurrence of the metabolic syndrome, its individual components and determining the factors influencing its development in Polish nurses. The research conducted among the nurses in question included DXA (Dual Energy X-ray Absorptiometry) measurements, assessment of glucose concentration, lipid profile, blood pressure and a questionnaire survey. Almost half of the surveyed nurses have metabolic syndrome, which significantly increases the risk of developing cardiovascular diseases or diabetes. After multivariate analysis, it was found that being overweight and obesity were significant factors influenced the MS (metabolic syndrome) occurrence among Polish nurses. Being overweight increases the chances of MS occurrence 8.58 times in relation to BMI (Body Mass Index) <25, obesity increases the chances of MS occurrence 8.085 times in relation to BMI <25, and obesity class II/III increases the chances of MS occurrence 16.505 times in relation to BMI <25. Preventive and supportive measures for this professional group are needed.

scholarly journals Emerging roles of C1Q tumor necrosis factor-related proteins in metabolic diseases

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Manjunath Ramanjaneya ◽  
Jayakumar Jerobin ◽  
Ilham Bettahi ◽  
Kodappully Sivaraman Siveen ◽  
Abdul-Badi Abou-Samra
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Metabolic Disorders ◽  
Pharmacological Intervention ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Related Proteins ◽  
Necrosis Factor

AbstractObesity and insulin resistance are key elements of the metabolic syndrome, which includes type 2 diabetes (T2D), dyslipidemia, systemic inflammation, hypertension, elevated risk for cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS). C1Q Tumor necrosis factor-related proteins (CTRPs) have recently emerged as important regulators of metabolism as a core component in the interrelationship between insulin resistance, adiposity and inflammation. To date 15 CTRP members have been identified and most of the CTRPs are dysregulated in obesity, T2D, coronary artery disease and NAFLD. Pharmacological intervention and lifestyle modification alter expression of CTRPs in circulation and in metabolically active tissues. CTRPs enhance metabolism mainly through activation of AMPK/AKT dependent pathways and possess insulin sensitizing properties. Thus dysregulated expression of CTRPs in metabolic disorders could contribute to the pathogenesis of the disease. For these reasons CTRPs appear to be promising targets for early detection, prevention and treatment of metabolic disorders. This review article aims at exploring the role of CTRPs in metabolic syndrome.

scholarly journals Homeostasis model assessment of insulin resistance (HOMA-IR) and metabolic syndrome at baseline of a multicentric Brazilian cohort: ELSA-Brasil study

2020 ◽  
Vol 36 (8) ◽  
Author(s):  
Maria de Fátima Haueisen Sander Diniz ◽  
Alline Maria Rezende Beleigoli ◽  
Maria Inês Schmidt ◽  
Bruce B. Duncan ◽  
Antônio Luiz P. Ribeiro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Normal Weight ◽  
Overweight And Obesity ◽  
Model Assessment ◽  
Adult Health ◽  
Homeostasis Model Assessment ◽  
The Metabolic Syndrome ◽  
Brazilian Cohort ◽  
Overweight Or Obesity

Abstract: Homeostasis model assessment of insulin resistance (HOMA-IR) is a method to measure insulin resistance. HOMA-IR cut-offs for identifying metabolic syndrome might vary across populations and body mass index (BMI) levels. We aimed to investigate HOMA-insulin resistance cut-offs that best discriminate individuals with insulin resistance and with metabolic syndrome for each BMI category in a large sample of adults without diabetes in the baseline of the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Among the 12,313 participants with mean age of 51.2 (SD 8.9) years, the prevalence of metabolic syndrome was 34.6%, and 60.1% had overweight or obesity. The prevalence of metabolic syndrome among normal weight, overweight and obesity categories were, respectively, 13%, 43.2% and 60.7%. The point of maximum combined sensitivity and specificity of HOMA-IR to discriminate the metabolic syndrome was 2.35 in the whole sample, with increasing values at higher BMI categories. This investigation contributes to better understanding HOMA-IR values associated with insulin resistance and metabolic syndrome in a large Brazilian adult sample, and that use of cut-off points according to ROC curve may be the better strategy. It also suggests that different values might be appropriate across BMI categories.

Growth factor regulation of uncoupling protein-1 mRNA expression in brown adipocytes

2002 ◽  
Vol 282 (1) ◽  
pp. C105-C112 ◽  
Author(s):  
Bibian García ◽  
Maria-Jesús Obregón
Keyword(s):  
Growth Factor ◽  
Adipocyte Differentiation ◽  
Uncoupling Protein ◽  
Brown Adipocyte ◽  
Mrna Levels ◽  
Uncoupling Protein 1 ◽  
Brown Adipocytes ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Continuous Presence

To study the effect of the mitogens epidermal growth factor (EGF), acidic and basic fibroblast growth factors (aFGF and bFGF), and vasopressin on brown adipocyte differentiation, we analyzed the expression of uncoupling protein-1 (UCP-1) mRNA. Quiescent brown preadipocytes express high levels of UCP-1 mRNA in response to triiodothyronine (T3) and norepinephrine (NE). The addition of serum or the mitogenic condition aFGF + vasopressin + NE or EGF + vasopressin + NE decreases UCP-1 mRNA. A second addition of mitogens further decreases UCP-1 mRNA. Treatment with aFGF or bFGF alone increases UCP-1 mRNA, whereas the addition of EGF or vasopressin dramatically reduces UCP-1 mRNA levels. The continuous presence of T3 increases UCP-1 mRNA levels in cells treated with EGF, aFGF, or bFGF. The effect of T3 on the stimulation of DNA synthesis also was tested. T3 inhibits the mitogenic activity of aFGF and bFGF. In conclusion, mitogens like aFGF or bFGF allow brown adipocyte differentiation, whereas EGF and vasopressin inhibit the differentiation process. T3 behaves as an important hormone that regulates both brown adipocyte proliferation and differentiation.

Sign in / Sign up

Export Citation Format

Share Document