Pathophysiology of Metabolic Syndrome: Part I—Influence of Adiposity and Insulin Resistance

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.

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

CNS & Neurological Disorders - Drug Targets ◽

10.2174/187152711799219271 ◽

2011 ◽

Vol 10 (8) ◽

pp. 921-927 ◽

Cited By ~ 9

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

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Metabolic Syndrome and Insulin Resistance in Schoolchildren From a Developing Country

Frontiers in Nutrition ◽

10.3389/fnut.2020.00031 ◽

2020 ◽

Vol 7 ◽

Author(s):

Rashmi Ranjan Das ◽

Manaswini Mangaraj ◽

Sandeep Kumar Panigrahi ◽

Amit Kumar Satapathy ◽

Samarendra Mahapatro ◽

...

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Developing Country

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Dual-specificity phosphatase 3 deletion promotes obesity, non-alcoholic steatohepatitis and hepatocellular carcinoma

Scientific Reports ◽

10.1038/s41598-021-85089-6 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Sophie Jacques ◽

Arash Arjomand ◽

Hélène Perée ◽

Patrick Collins ◽

Alice Mayer ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Insulin Resistance ◽

Metabolic Syndrome ◽

Liver Damage ◽

Chow Diet ◽

Serum Triglycerides ◽

Alcoholic Fatty Liver ◽

Alcoholic Steatohepatitis ◽

Dual Specificity ◽

Dual Specificity Protein Phosphatase

AbstractNon-alcoholic fatty liver disease (NAFLD) is the most common chronic hepatic pathology in Western countries. It encompasses a spectrum of conditions ranging from simple steatosis to more severe and progressive non-alcoholic steatohepatitis (NASH) that can lead to hepatocellular carcinoma (HCC). Obesity and related metabolic syndrome are important risk factors for the development of NAFLD, NASH and HCC. DUSP3 is a small dual-specificity protein phosphatase with a poorly known physiological function. We investigated its role in metabolic syndrome manifestations and in HCC using a mouse knockout (KO) model. While aging, DUSP3-KO mice became obese, exhibited insulin resistance, NAFLD and associated liver damage. These phenotypes were exacerbated under high fat diet (HFD). In addition, DEN administration combined to HFD led to rapid HCC development in DUSP3-KO compared to wild type (WT) mice. DUSP3-KO mice had more serum triglycerides, cholesterol, AST and ALT compared to control WT mice under both regular chow diet (CD) and HFD. The level of fasting insulin was higher compared to WT mice, though, fasting glucose as well as glucose tolerance were normal. At the molecular level, HFD led to decreased expression of DUSP3 in WT mice. DUSP3 deletion was associated with increased and consistent phosphorylation of the insulin receptor (IR) and with higher activation of the downstream signaling pathway. In conclusion, our results support a new role for DUSP3 in obesity, insulin resistance, NAFLD and liver damage.

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