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Summary

This chapter discusses the pathogenesis, diagnosis and therapeutic strategies for metabolic syndrome, which can generally be defined as the coexistence of increased adiposity/obesity, hypertension, dyslipidemia (high serum triglyceride and/or low serum HDL levels), and/or hyperglycemia/insulin resistance. Various definitions of this syndrome specify the requirement of at least 2-3 of these factors, all of which substantially increase the risk of atherosclerotic disease. A large proportion of the global adult population (20-35%, depending on the definition used) are thought to have metabolic syndrome. Lifestyle, particularly sedentary behaviour, has a dominant role in the pathogenesis of this syndrome, but environmental and biological factors also contribute (see accompanying Hurst's Central Illustration). Therapeutic strategies, which should be applied early, normally involve a combination of lifestyle as well as pharmacological and/or procedural interventions.

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eFig 26-01

Hurst's Central Illustration: The Metabolic Syndrome

Factors that contribute to the pathogenesis, diagnosis and therapeutic strategies for metabolic syndrome. *Various guidelines require the coexistence of at least 2-3 of these factors.

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INTRODUCTION

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The metabolic syndrome (MetS) is a theoretic construct from clustering of interrelated processes to better represent complex pathophysiology into actionable and effective clinical decision making. Specifically, the rationale and practical utility of MetS is to facilitate early diagnosis, risk stratification, and management of cardiometabolic risk factors. This topic is relevant but also remains controversial because many aspects remain unproven. Nevertheless, the core principle is that the value of MetS is related to the impact of residual risk (total risk minus the aggregate of known specific risk factors) on cardiovascular disease (CVD). A recent consensus statement has advanced the discussion and relevance of MetS by proposing different subtypes and severity levels in the context of a public health care model.1

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Energy homeostasis is coordinated by hormone signal pathways that integrate the metabolic activities of multiple tissues and organ systems. Insulin resistance disrupts metabolic efficiency, thereby driving many chronic metabolic diseases, including type 2 diabetes (T2D), atherosclerosis, hypertriglyceridemia, hepatosteatosis, polycystic ovary syndrome, and obesity. Informally, insulin resistance may also be classified as prediabetes. As a common pathophysiologic pathway, insulin resistance affects and is affected by metabolism in adipose tissue, skeletal muscle, vascular endothelium, bone, liver, kidneys, pancreatic islets of Langerhans, hypothalamic nuclei, and the immune system.

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In general, the diagnosis of MetS is based on the complex of increased adiposity/obesity, hypertension, hypertriglyceridemia, and insulin resistance.1 The prevalence of MetS varies depending on the specific definition used (Table 26–1)2,3,4,5,6,7 but has nevertheless increased substantially over the past few decades in parallel to the rise in obesity. This rise is associated with modern (westernized) lifestyles, food preferences and availability, agricultural changes, environmental exposures, and other related epigenetic factors. Depending on the specific criteria used, approximately 20% to 35% of various reported worldwide adult populations have ...

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