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A multitude of pathophysiological cardiometabolic variables have been correlated with the severity of cardiovascular events. The variance of fat cells is a critical aspect of cardiometabolic risk. The cardiac syndrome's most prominent interpretation is abdominal obesity. Adipose tissue is also an endocrine organ that expels adipokines which make a contribution to the atherogenic/diabetic physiological risk level attributed to hyperlipidaemia. A mismatch between energy consumption and expenditure contributes to abdominal fat. The pathogenicity of hyperglycaemia and hyperlipidaemia correlated with the cardiometabolic syndrome is probably triggered by variations in free fatty acid metabolism. It is a metabolically active tissue that metabolises a number of up‐regulation and thrombogenic immune cells. Elevated plasma unsaturated fatty acid accumulation and inordinate release of lipids from adipocytes can hinder the ability of insulin to stimulate muscle glucose metabolism and suppress hepatic glucose production (Figure 2.2) (Kirk and Klein 2009). In juveniles, insulin tolerance tends to be related to a decline in the mitochondrial to nuclear DNA ratio. Elevated secretion of lipids from adipocytes is attributed to insulin sensitivity leading to a decline in glucose transmission through the muscles (Gill et al. 2005). Hyperinsulinemia has been reported as a significant prognostic factor in broad prospective epidemiologic trials. In conclusion, there is considerable proof that the most prevalent forms of the metabolic syndrome are correlated to abdominal obesity, especially when it is followed by abdominal adipocytes accumulation.

Figure 2.2 Dysregulation of sugar metabolism leads to cardiometabolic syndrome.

Source: Based on Kirk and Klein (2009).