Endocrine Diseases in Diabetes Mellitus

Abstract

The endocrine pancreas secretes several hormones including insulin and glucagon and dysfunction of them may lead to diabetes mellitus. The integrated regulation of systemic glucose balance prevents the devastating consequences of hypoglycemia and hyperglycemia. This remarkable homeostatic feat is accomplished primarily by hormones, but also by neurotransmitters and substrate effects, and it reflects the interplay of plasma glucoselowering and glucose-raising factors. Moreover, endocrine diseases frequently co-associate with diabetes mellitus. There have also been several reports on changes in growth hormone (GH) in nutrient excess or deprivation. GH is released into the general circulation where it interacts with multiple peripheral tissues through its receptor, GH receptor, to regulate growth and metabolic function. In humans, GH levels decrease in states of nutrient excess such as obesity, and increase in response to nutrient deprivation such as fasting. Considering that GH regulates metabolism of carbohydrate, lipid, and protein, clarifying the mechanisms by which metabolic changes alter GH synthesis and secretion will increase our knowledge on the pathophysiology and treatment of metabolic diseases. In this review, the effect of nutrient excess and nutrient deficiency on GH axis function in hu mans will be summarized, with particular emphasis on studies exploring the direct effects of systemic signals, including insulin-like growth factor 1 (IGF-1) and insulin, on somatotrope function. Moreover, there will be a discussion over the overlap syndrome consisting of multiple endocrine neoplasm (MEN) and polyglandular autoimmune diseases (PGA).