Glucose/Insulin Homeostasis

Key Points

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• Glucose is abundant in a wide range of foods. In the fasted state, the liver provides the bulk of glucose to the bloodstream through glycogenolysis and gluconeogenesis.
• Insulin optimizes glucose uptake by skeletal muscle, its major peripheral user. Insulin also reduces liver glucose production after a meal and reduces fatty acid release by adipose tissue. These three major functions are important for glucose homeostasis.
• Expansion of intra-abdominal (visceral) fat causes adipocyte hypertrophy. This process triggers macrophages that, together with the enlarged adipocytes, locally secrete insulin-resistance-promoting molecules.
• Hypertrophied insulin-resistant intra-abdominal adipocytes release more fatty acids and proinflammatory adipokines into the bloodstream. The portal circulation carries these to the liver where they promote steatosis, insulin resistance, and local inflammation. The systemic circulation carries fatty acids and proinflammatory molecules to skeletal muscle where they promote lipid accumulation, insulin resistance, and local inflammation.
• Insulin resistance also affects the function of other systems and organs, including endothelial cells and cells of the vascular wall. This further increases CVD risk.
• Insulin resistance is believed to play a role in the development of many metabolic abnormalities that define the metabolic syndrome. It is also believed to be a strong link between intra-abdominal obesity and increased risk of type 2 diabetes and CVD.
• Targeting the fundamental cause of obesity-related insulin resistance by reducing intra-abdominal fat mass remains an important therapeutic objective.
  

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