Obesity and insulin resistance correlation are still being determined. However, metabolic syndrome shows a greater risk of insulin resistance, obesity, and type 2 diabetes. Adipose tissue (fat cells) is prone to insulin resistance and increases with fat mass. The specific link between insulin resistance and visceral adipose tissue (fat) is still being determined. Visceral fat is also more prone to chronic inflammation and overproduction of inflammatory cytokines, which contribute to insulin resistance.
Over the past several years, there have been some reports of increased insulin resistance, obesity, and type 2 diabetes in humans, particularly those of Asian origin. One mechanism involved in the increased risk of these diseases may be the observation that humans lacking the enzyme pancreatic insulin sensitivity have a high prevalence of insulin-resistant syndrome, obesity, and diabetes. In a recent study performed on rodents, they showed it that the pancreatic enzyme Trpflaminic acid decreased in the presence of green tea but increased in its absence.
Another mechanism involved in obesity and insulin resistance correlation is the effect of lipogenesis on insulin receptor signalling. Lipogenesis, or the ability of cells to form or secret lipids, occurs when carbohydrate intake increases. When there is an increase in the rate of lipogenesis, the rate of insulin secretion also increases. Lipogenesis negatively affects insulin receptors, which is why people with fatty acid signalling defects have higher rates of insulin resistance and obesity.
Obesity and Insulin Resistance Correlation
Endocrine dysfunctions such as the growth hormone, thyroid disorder, cystic fibrosis, and pancreatic tumour impair insulin receptor signalling and thus increase the risk of obesity and insulin resistance. Fatty tissue accumulation within adipose cells of obese individuals also influences the functioning of the hypothalamus and pituitary gland. Obesity and insulin resistance have links.
A third mechanism of obesity and insulin resistance is the impairment of glucose transport by the skeletal muscle. Exercise prevents the accumulation of fat within the muscle tissues, and it decreases the rate of glycolysis, which is the process through which they metabolize glucose. Therefore, the insulin resistance and obesity correlation are not only because of the accumulation of fat within the body but also because of the decrease of energy available to the muscle tissues. Obesity and diabetes have common characteristics of reduced activity of the skeletal muscles. And the impairment of glucose transport and energy metabolism is the most likely cause of these syndromes. They have shown it that insulin resistance and obesity relate to each other because muscle loss in diabetic conditions causes an increase in blood glucose levels.
They decrease the fourth mechanism implicated in obesity and insulin resistance activity of the adipose cells. This reduced activity of the adipose cells may occur because of the excessive accumulation of fat in the abdominal area. When blood glucose levels decrease in obese people, the adipose cells release a hormone called adiponectin. The adiponectin stimulates the production of glucose by the liver, and this increased glucose intake stimulates obesity and types 2 diabetes. The decreased activity of the adipose cells may also be because of the impaired accessibility of fatty tissue to the insulin receptors in their vicinity.