Body composition is a good indicator of metabolic health. Yet body mass index is less so as weight does not account for the percentage of body fat.
Obesity is caused by energy intake being greater than energy expenditure. With weight gain, decreased insulin sensitivity is detected and weight loss shows increased insulin sensitivity.
Metabolically healthy is defined as the absence of T2DM, HTN, dislipidemia. 10-25% of obese individuals are considered metabolically healthy. Kloting et al., (2010) assessed insulin sensitivity in metabolically healthy individuals yet those who were insulin resistant (IR) had a higher fasting plasma glucose, fasting triglycerides and higher fasting HDL.
Goossens et al., (2011) noted that obesity shows fat cell enlargement and is related to IR and T2DM. Showing this is an independent marker of IR, it does predict T2DM.
Obesity causes Hypertropic adipocytes which gives altered adipokine secretion by the adipose tissue. The release of cytokines has an effect on the cells around them. These cell signalling proteins such as Leptin and interleukin-6 are altered. Hypertropic adipocytes are already overloaded with stored triglycerides. Lipids can spill over into the circulation, affecting the liver, heart, skeletal muscle.
Macrophages increase in percentage in adipose tissue when those obese individuals are IR compared to those obese only. Therefore the size of the fat cell is important. As liposuction does not have an effect on the rate of IR, we know it is not the quantity of adipose tissue rather the size of the adipocytes.
Adipose tissue is known to secrete a large number of proteins which regulate metabolism, energy intake and fat storage. Activation of the (adaptive) immune system is considered the primary event of adipose tissue inflammation. It occurs before the hypertrophy of adipocytes and has been shown to play a major role in the recruitment and activation of macrophages (Stolarczyk, 2017.) Currently the activation of macrophages is thought to be a metabolic and immune process.
Obesity can induce systemic oxidative stress through oxidative phosphorylation. Causing low antioxidant defence, chronic inflammation and hyperleptinemia. Weight reduction decreases oxidation markers, endothelial disfunction and impaired mitochondrial disfunction (Manna, 2015).
Trayhurt and Wood, (2004), asked what triggers hypertrophic adipocytes. They discussed the hypoxia hypothesis which showed the formation of new blood vessels (angiogenesis) isn't sufficient in adipose tissue therefore the tissue will be oxygen deficit. This study in rats was proven yet not quite so conclusive yet in humans.
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