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Mill Creek Keto Obesity is a disease associated with significant abnormalities of the endocrine glands. Hyper-insulinemia and insulin resistance are the two most well-known alterations. Although their mechanisms of action and clinical significance are unclear

In addition, obesity is defined as excess body fat. Its clinical management is complex and often gives poor results. Abdominal obesity, otherwise known as central obesity, reflects the amount of visceral fat and is directly related to insulin resistance and cardiovascular events.

Both obesity and overweight lead to a series of endocrine and metabolic alterations. Most of these changes are secondary to obesity as they can be induced by overeating and eliminated with weight loss.

The main glands of the endocrine system are the hypothalamus, pituitary , thyroid gland, parathyroid glands, pancreas, adrenal glands and gonads (testes for men and ovaries for women).

These endocrine glands secrete chemicals called hormones when needed. They help regulate a large amount of cellular activities, such as:

The most characteristic endocrine disruption of obesity is the increased secretion of insulin. This is because obese people have higher insulin concentrations. Concretely, the secretion of basal and assimilated insulin over 24 hours is 3 or 4 times higher in obese subjects than in thin subjects.

Both obesity and type 2 diabetes mellitus are linked to insulin resistance. However, most insulin - resistant obese people do not develop hyperglycemia .

In short, hyperinsulinemia is common in obesity. However, insulin resistance is characteristic when there is a large weight load.

As we already know, the pituitary gland is one of the main endocrine glands in the body. In obesity, the most marked alteration in the functioning of this gland is linked to growth hormone or GH.

The secretion of this hormone depends, above all, on the interaction between somatocrinin (GHRH) and somatostatin (GIH). In obesity, there is a decrease in the secretion of GH.

On the other hand, in children and adults, the higher the body mass index, the less growth hormone reacts to various secretory stimuli. It has been shown that for every unit of body mass index - or BMI - at a certain age, GH secretion decreases by up to 6%.

Obesity and the “gonad” endocrine glands

First of all, we need to differentiate between the female gonads, the ovaries , and the male gonads, the testes.

Regarding the relationship between obesity and the endocrine glands, this disease manifests itself in women by a set of conditions that precede metabolic abnormalities like prediabetes and cardiovascular disease. These anomalies include:

Furthermore, at the end of a woman's reproductive life, the cessation of ovarian function is also associated with the development of obesity. Indeed, menopause precipitates abdominal weight gain, in connection with many adverse metabolic consequences.

As for humans, obesity is linked to the reduction in total testosterone. The pathogenic factors which intervene are the decrease in the capacity of union of the globulins binding the sex hormones, the reduction in the amplitude of the impulses of LH or “luteinizing” hormone and the hyperestrogenism.

On the other hand, LH is the hormone that regulates the secretion of testosterone. It acts on the cells of the testes and stimulates the production Mill Creek Keto of testosterone.

Obesity and the adrenal glands

Given the relationship between obesity, central fat distribution and hypercholesterolemia, many studies have attempted to determine the relevant role of cortisol in the development of obesity in the general population.

In obese women with abdominal fat distribution, the rate of urinary free cortisol were significantly increased compared to women without this problem. Therefore, these results suggest that these women have hyperactivity in the hypothalamus-pituitary-adrenal axis.

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