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Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences.

ABSTRACT: The prevalence of sarcopenic obesity is increasing worldwide, particularly amongst aging populations. Insulin resistance is the core mechanism of sarcopenic obesity and is also associated with variable cardiometabolic diseases such as cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. Fat accumulation in muscle tissue promotes a proinflammatory cascade and oxidative stress, leading to mitochondrial dysfunction, impaired insulin signaling, and muscle atrophy. To compound the problem, decreased muscle mass aggravates insulin resistance. In addition, the crosstalk between myokines and adipokines leads to negative feedback, which in turn aggravates sarcopenic obesity and insulin resistance. In this review, we focus on the molecular mechanisms linking sarcopenic obesity and insulin resistance with various biological pathways. We also discuss the impact and mechanism of sarcopenic obesity and insulin resistance on cardiometabolic disease.

SUBMITTER: Hong SH

PROVIDER: S-EPMC7013734 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences.

Hong So-Hyeon SH Choi Kyung Mook KM

International journal of molecular sciences 20200113 2

The prevalence of sarcopenic obesity is increasing worldwide, particularly amongst aging populations. Insulin resistance is the core mechanism of sarcopenic obesity and is also associated with variable cardiometabolic diseases such as cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. Fat accumulation in muscle tissue promotes a proinflammatory cascade and oxidative stress, leading to mitochondrial dysfunction, impaired insulin signaling, and muscle atrophy. ...[more]

PMID: 31941015

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Project description:The prevalence of obesity has increased globally over the last 2 decades. Although the body mass index has been a convenient and simple index of obesity at the population level, studies have shown that obesity defined by body mass index alone is a remarkably heterogeneous condition with varying cardiovascular and metabolic manifestations across individuals. Adipose tissue is an exquisitely active metabolic organ engaged in cross-talk between various systems; perturbation of adipose tissue results in a pathological response to positive caloric balance in susceptible individuals that directly and indirectly contributes to cardiovascular and metabolic disease. Inadequate subcutaneous adipose tissue expansion in the face of dietary triglycerides leads to visceral and ectopic fat deposition, inflammatory/adipokine dysregulation, and insulin resistance. Conversely, preferential fat storage in the lower body depot may act as a metabolic buffer and protect other tissues from lipotoxicity caused by lipid overflow and ectopic fat. Translational, epidemiological, and clinical studies over the past 30 years have clearly demonstrated a strong link between visceral and ectopic fat and the development of a clinical syndrome characterized by atherogenic dyslipidemia, hyperinsulinemia/glucose intolerance, hypertension, atherosclerosis, and adverse cardiac remodeling/heart failure. This relationship is even more nuanced when clinical entities such as metabolically healthy obesity phenotype and the obesity paradox are considered. Although it is clear that the accumulation of visceral/ectopic fat is a major contributor to cardiovascular and metabolic risk above and beyond the body mass index, implementation of fat distribution assessment into clinical practice remains a challenge. Anthropometric indexes of obesity are easily implemented, but newer imaging-based methods offer improved sensitivity and specificity for measuring specific depots. Lifestyle, pharmacological, and surgical interventions allow a multidisciplinary approach to overweight/obesity that may improve outcomes and align with a public health message to combat the growing epidemic of obesity worldwide and to build healthier lives free of cardiovascular diseases.

Project description:This study assessed the effect of obesity on metabolic and cardiovascular disease risk factors in HIV-infected adults on antiretroviral therapy with sustained virologic suppression.Observational, comparative cohort study with three group-matched arms: 35 nonobese and 35 obese HIV-infected persons on efavirenz, tenofovir and emtricitabine with plasma HIV-1 RNA ?less than ?50? copies/ml for more than 2 years, and 30 obese HIV-uninfected controls. Patients did not have diabetes or known cardiovascular disease.We compared glucose tolerance, serum lipids, brachial artery flow-mediated dilation, carotid intima-media thickness, and soluble inflammatory and vascular adhesion markers between nonobese and obese HIV-infected patients, and between obese HIV-infected and HIV-uninfected patients, using Wilcoxon rank-sum tests and multivariate linear regression.The cohort was 52% men and 48% nonwhite. Nonobese and obese HIV-infected patients did not differ by clinical or demographic characteristics. Obese HIV-uninfected controls were younger than obese HIV-infected patients and less likely to smoke (P?<?0.03 for both). Among HIV-infected patients, obesity was associated with greater insulin release, lower insulin sensitivity, and higher serum high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-? receptor 1 levels (P?<?0.001), but similar lipid profiles, sCD14, sCD163, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1, and carotid intima-media thickness and flow mediated dilation. In contrast, Obese HIV-infected patients had adverse lipid changes, and greater circulating intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and sCD14, compared with obese HIV-uninfected controls after adjusting for age and other factors.Obesity impairs glucose metabolism and contributes to circulating high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-? receptor 1 levels, but has few additive effects on dyslipidemia and endothelial activation, in Obese HIV-infected adults on long-term antiretroviral therapy.

Dataset Information

Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences.

Publications

Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences.

Similar Datasets

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