Pubertal Changes in Insulin Secretion and Peripheral Insulin Sensitivity

Abstract

Using a simple and standardized method we estimated both insulin secretion and insulin sensitivity in peripheral tissues in relation to Tanner pubertal stages. Early insulin response, mean blood glucose (MBG), mean serum insulin (MSI), glucose uptake rate in peripheral tissues and insulin sensitivity index (SI) in response to the standard oral glucose tolerance test were evaluated in 73 normal girls. Study subjects were divided into 4 groups: group 1 (Tanner stage I, n = 20); group 2 (Tanner stage II, n = 14); group 3 (Tanner stages III and IV, n = 15), and group 4 (Tanner stage V, n = 24). Steroid levels and insulin-like growth factors were determined to characterize clinical pubertal development. MBG was similar in all groups but MSI increased at stage II and retained similar values throughout puberty, with those of group I being statistically lower than in the other groups (p < 0.001). When MSI values were adjusted per kilogram of body weight, a significant increase was observed in group II (p < 0.05). The MSI adjusted values were: group 1 1.0 ± 0.4; group 2, 1.4 ± 0.4; group 3, 1.0 ± 0.3, and group 4, 1.0 ± 0.4 mU/l/kg. SI values were similar in groups 1 and 2 and significantly lower than in groups 3 and 4 (p < 0.001). Our results confirm both that insulin secretion is related to age and that an insulin-resistant state occurs during puberty. Thus, the insulin-resistant state coincides with Tanner stage II. In conclusion, this mathematical approach is considered to be a simple and reliable method for analyzing the possible alterations in insulin secretion and action in children and adolescents in whom more sophisticated procedures must be limited in this early period of life for ethical reasons.

Liver steatosis in juvenile obesity: correlations with lipid profile, hepatic biochemical parameters and glycemic and insulinemic responses to an oral glucose tolerance test

“…This suggests a compensatory effect secondary to the augmented insulin resistance occurring during the pubertal development, as previously reported. 34,46 However, we found no differences between subjects with and without steatosis, a fact that leads us to assume that in obese adolescents, steatosis is not associated with a pancreatic insulin hypersecretion, as suggested in some experimental models. 28 In conclusion, ultrasound scanning shows a greater percentage of liver damage than that recognized by the increase of serum levels of biochemical parameters, among which ALT is the most altered one; steatosis is associated with a tendency to an increase of TGL and a decrease of HDL in late puberty, whereas alterations of insulin secretion do not seem to be involved in this condition during the pubertal development.…”

Threshold value of subepicardial adipose tissue to detect insulin resistance in obese children

“…30 In addition to these changes during puberty, physiological insulin resistance was reported in a number of studies. [31][32][33] It has been shown that insulin resistance increases significantly by T2, remains constant between T2 and T4, and returns almost to T1 levels by the end of puberty (T5). 34 All of the abovementioned findings shed light on the effects of puberty on BMI and insulin resistance; however, to the best of our knowledge, we did not encounter a study evaluating the effects of puberty on SAT.…”

Sexual dimorphism in the maturation of the pituitary-gonadal axis, assessed by GnRH agonist challenge

“…Serum testosterone, estradiol, 17-OHP, DHEAS, D 4 -A and SHBG levels were measured by RIA, as described (15). Serum IGF-I was determined by RIA after acid extraction and protein saturation by IGF-II (Nichols Institute Diagnostics, San Juan Capistrano, CA, USA), and IGFBP-1 and IGFBP-3 were determined using a commercially available kit (DSL, Webster, TX, USA) (16).…”