Puberty decreases insulin sensitivity

Bloch, C; Clemons, Peter; Sperling, Mark A.

doi:10.1016/s0022-3476(87)80522-x

Cited by 358 publications

(220 citation statements)

References 24 publications

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“…Higher insulin resistance during puberty has been found to be mediated by these factors, independent of body fat mass (46)(47)(48)(49). Likewise, our observations in Bogalusa children showed that increases in sex hormones and IGF-1 during puberty adversely influence lipoprotein and blood pressure levels, independent of adiposity (50,51).…”

Section: W Chen and Associatessupporting

confidence: 66%

Age-related patterns of the clustering of cardiovascular risk variables of syndrome X from childhood to young adulthood in a population made up of black and white subjects: the Bogalusa Heart Study.

et al. 2000

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The age-related patterns of clustering of cardiovascular risk variables of Syndrome X from childhood to adulthood were examined in a community-based sample of black and white children (aged 5-10 years, n = 2,389), adolescents (aged 11-17 years, n = 3,371), and young adults (aged 18-37 years, n = 2,115). In the analysis of clustering, insulin resistance index, BMI, triglycerides/ HDL cholesterol ratio, and mean arterial pressure were used either as categorical variables (age-, race-and sexspecific values >75th percentiles) to calculate risk ratios (observed frequency/expected frequency) or as continuous variables (normal scores based on ranks) to compute intraclass correlations. In the total sample, the risk ratio for clustering of adverse levels of all 4 variables was 9.8 for whites (P < 0.01) versus 7.4 for blacks (P < 0.01); the intraclass correlation was 0.33 for whites (P < 0.001) versus 0.26 for blacks (P < 0.001). Both the risk ratio and intraclass correlation were significantly higher in whites than in blacks in the total sample. The intraclass correlations of the 4 variables were significant (P < 0.001) in all race and age-groups, and they were higher during preadolescence and adulthood than during adolescence. Furthermore, unlike risk ratios, intraclass correlations showed a continuous increase with age during adulthood. When BMI was adjusted, the intraclass correlations involving the other 3 variables were reduced by ~50%, and the age-related pattern was no longer evident. These results suggest that the degree of clustering of risk variables of Syndrome X varies with age from childhood to adulthood and is likely influenced by the age-related changes in obesity and the attendant insulin resistance. Diabetes 49:1042-1048, 2000 D yslipidemia, hypertension, hyperinsulinemia, and obesity have been recognized as potent risk factors for coronary heart disease in adults (1-3). These risk factors have also been found to be associated with early atherosclerotic lesions in youth (4,5). Further, the extent of coronary atherosclerosis in youth increased markedly with the number of multiple risk factors (6). Coexistence of the above cardiovascular risk variables often occurs in both children (7-10) and adults (7,8,(11)(12)(13). Such a condition has been termed Syndrome X (14), deadly quartet (15), insulin resistance syndrome (11,16), and multiple metabolic syndrome (17).Although the clustering of cardiovascular risk factors related to Syndrome X has been found to occur at a very early age (7-10) and persist from childhood into adulthood (8), very little is known about the age-related trend in clustering of risk variables during this period. The Bogalusa Heart Study, a long-term community-based investigation of cardiovascular disease risk factors in black and white children and young adults (18)(19)(20), provided a unique opportunity to examine the age-related trend in clustering of risk variables during this period. The objective of the present study was to determine the age-related patterns in the magnitude of clus...

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Section: W Chen and Associatessupporting

confidence: 66%

Age-related patterns of the clustering of cardiovascular risk variables of syndrome X from childhood to young adulthood in a population made up of black and white subjects: the Bogalusa Heart Study.

et al. 2000

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“…9 It is well-known that puberty causes a transient reduction in insulin sensitivity in normal subjects. 28,29 At the last evaluation, our subjects had completed pubertal development and therefore this confounding effect was lost. IAT seems to act differently at different ages.…”

Section: Discussionmentioning

confidence: 99%

Persisting obesity starting before puberty is associated with stable intraabdominal fat during adolescence

et al. 1999

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OBJECTIVES: To observe the evolution of intraabdominal adipose tissue (IAT) in obese prepubertal children, who did not change their degree of obesity during adolescence and to evaluate its relationship with metabolic risk indexes (RI). DESIGN: Longitudinal study of 16 obese adolescents (eight male and eight female) in whom relative body weight (RBW) did not change signi®cantly and pubertal development was completed during the study period. MEASUREMENTS: Magnetic resonance imaging (MRI) scan at lumbar level (L4) three times during a 4 y period. At basal and at four years biochemical assays for metabolic indexes. RESULTS: IAT did not differ signi®cantly over the three measurement times and showed signi®cant correlations between ®rst and second (r 0.66, P`0.005), ®rst and third (r 0.61, P`0.01) and second and third values (r 0.84, P`0.0001). Subcutaneous adipose tissue (SAT) increased signi®cantly from basal to third evaluation (P`0.002). At baseline, IAT correlated signi®cantly with lipids (total and LDL cholesterol r 0.72, P`0.004), while at the end of the study, IAT correlated positively with insulin (fasting insulin r 0.55, P`0.008, insulin area after oral glucose tolerance test (OGTT) r 0.60, P`0.03, fasting insulinaglucose r 0.67 P`0.006) and negatively with high density lipoprotein (HDL) cholesterol (r 7 0.55, P`0.04). CONCLUSIONS: Obesity achieved before puberty, and stable during adolescence, showed a relatively stable amount of IAT. In post pubertal children the relationship of IAT to clinically signi®cant risk factors resemble the pattern in obese adults.

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“…(34) At the onset of puberty, increased pulsatile growth hormone (GH) secretion results in insulin resistance and compensatory hyperinsulinemia which in turn stimulate the growth spurts. (35)(36)(37) Insulin resistance with compensating hyperinsulinism is also a common feature of PCOS. The increased serum insulin levels further decrease hepatic synthesis of IGFBP-1 and in turn enhance the bioactivity of IGF-I.…”

Section: Genetics and Pcosmentioning

confidence: 99%