Abstract
GH is one of the insulin counterregulatory hormones which acts in the opposite way to insulin, increasing the glucose production by the liver and kidneys and decreasing glucose uptake from peripheral tissues, thus being a hyperglycemic hormone. When in excess, as in acromegaly, it induces glucose intolerance and diabetes. As expected, patients with GH deficiency (GHD) have hypoglycemia, especially in early childhood, but as GH is also a lipolytic hormone, these patients are becoming obese with higher percentages of body fat. Although obesity in general is directly related to insulin resistance, in patients with GH secretion disorders this relationship may be altered. In acromegaly there is a decrease in fat mass with worsening insulin sensitivity and mice with isolated GHD are characterized by greater insulin sensitivity despite excess fat mass. In humans with GHD, body composition shows increased body fat and decreased free fat mass, but the results regarding insulin sensitivity are still controversial in these patients. These discrepant results regarding insulin sensitivity in patients with GHD suggest the existence of other variables influencing these results. In the present review, we will try to follow the path of the different researches conducted on this subject, both in animal and human models, with the goal of understanding the current knowledge of insulin sensitivity across the spectrum of GHD. Arch Endocrinol Metab. 2019;63(6):582-91.
Highlights
G H deficiency (GHD) is characterized by signs and symptoms resulting from decreased serum GROWTH HORMONE (GH) levels that vary according to the age of patient
The GH, known as somatotropic hormone or somatotropin, is a protein that contains 191 single chain amino acids with a molecular weight of 22.005 Kda [12]. It is produced by pituitary somatotrophs, and its secretion occurs in pulses that are controlled by the hypothalamus through GH-releasing hormone (GHRH), somatostatin and ghrelin [13,14]
Evaluation of insulin sensitivity (IS) by the euglycemic hyperinsulinemic clamp (EHC) method in patients with GHD showed that patients with onset of GHD in early life had better IS when compared with controls paired by sex, age, and BMI, while patients with hypopituitarism who started hormone deficiency later in life have IS similar to the control group, suggesting that adipose tissue that did not undergo the physiological action of GH during early childhood should be different from adipose tissue that experienced this action at this stage of life, since the former is more sensitive to insulin action, results not yet published [99]
Summary
G H deficiency (GHD) is characterized by signs and symptoms resulting from decreased serum GH levels that vary according to the age of patient. There is increased glucagon secretion by the pancreatic alpha cells, the hypothalamus stimulates the sympathetic nerve system and later both cortisol and GH are secreted in response to hypoglycemia These hormones decrease glucose uptake by peripheral tissues and increase glucose production in the liver and kidneys, helping to prevent hypoglycemia [10,11]. The GH, known as somatotropic hormone or somatotropin, is a protein that contains 191 single chain amino acids with a molecular weight of 22.005 Kda [12] It is produced by pituitary somatotrophs, and its secretion occurs in pulses that are controlled by the hypothalamus through GH-releasing hormone (GHRH), somatostatin and ghrelin [13,14]. IGF-I, known as somatomedine C, belongs to the IGF system, which consists of different elements: IGF-I and IGF-2, two receptor types: IGFR-1 and IGFR-2 and various binding proteins IGFBP 1 to 6
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