Changes in Insulin Resistance and Cardiovascular Risk During Adolescence

Abstract

Background— Developmental changes in insulin resistance and cardiovascular risk were studied in youths 11 to 19 years of age. Methods and Results— A cohort was randomly selected after blood pressure screening of Minneapolis, Minn, school children. Studies were done 3 times on this cohort and once on their siblings (996 observations on 507 individuals from 363 families). Insulin sensitivity was determined by euglycemic clamp. Body mass index and waist circumference increased similarly in both sexes from ages 11 to 19 years. Body fat decreased in males and increased in females ( P <0.001). Lean body mass increased at a steeper rate in males ( P <0.0001). Insulin resistance was lower in males at 11 years but increased steadily to 19 years ( P =0.003); in contrast, it did not increase in females. Thus, despite being less insulin resistant at 11 years and decreasing in fatness during puberty, males became more insulin resistant than females by 19 years of age. Triglycerides increased in males and high-density lipoprotein cholesterol decreased, whereas the opposite pattern was seen in females, which resulted in higher triglycerides and lower high-density lipoprotein cholesterol in males at 19 years. No gender difference in low-density lipoprotein or total cholesterol was seen. Systolic blood pressure increased in both sexes but at a greater rate in boys ( P =0.03). Conclusions— During the transition from late childhood through adolescence, insulin resistance in males increased in association with increased triglycerides and decreased high-density lipoprotein cholesterol, despite a concurrent reduction in body fatness, whereas the opposite occurred in females. These gender-related developmental changes in insulin resistance, which were independent from changes in fatness, total cholesterol, and low-density lipoprotein cholesterol, are consistent with an early role for insulin resistance in the increased cardiovascular risk found in males.

Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

“…Female sex during adolescence has been shown to exert a positive influence on insulin sensitivity, lipids and blood pressure (Moran et al 2008), which is in line with the notion that premenopausal women have a lower risk of developing the metabolic syndrome compared with age-matched men (Isomaa et al 2001, Legato et al 2006, Regitz-Zagrosek et al 2007. No single risk factor or combination of factors has yet been shown to fully explain this, but the fact that risk protection disappears after menopause strongly suggests that female hormones play a protective role.…”

Insulin resistance in young, lean male subjects with essential hypertension

“…1,2 It is known that similar to older individuals, HT in young age coexists with features of metabolic syndrome, such as overweight/obesity, hyperinsulinaemia/insulin resistance and dyslipidaemia. [3][4][5] It is even suggested that the pathophysiologic precursors of adult HT originate earlier in life.…”

“…5 However, an overall worsening of insulin sensitivity, lipid levels and blood pressure in adolescent male subjects may occur despite a minimal alteration in total body fat. 1 No studies have been carried out on these lean individuals on whether the presence of these risk factors, including HT, is owing to the preferential visceral deposition of adipose tissue, as documented by studies in overweight/obese subjects. [8][9][10] Despite fatness being associated with insulin resistance and HT, it is clear that obesity per se cannot fully explain the development of insulin resistance.…”

Determinants of birth weight in boys and girls

“…increased adiposity was more enhanced in female than male rat offspring (Bayol et al 2001). Boys at 19 years of age have a higher lean body mass than girls at the same age, but they also have higher prevalence of insulin resistance (Moran et al 2006). among children at the age of five, girls have higher insulin resistance human _ ontogenetic s than boys.…”