Effects of maturational stage on insulin sensitivity during puberty.

Cook, Jack; Hoffman, Robert P.; Stene, Mark; Hansen, Jørgen

doi:10.1210/jcem.77.3.7690363

Cited by 81 publications

(93 citation statements)

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“…It is very interesting that IR HOMA , which is a gross index of insulin resistance, showed the same patterns reported with the measure of glucose uptake with an accurate technique like euglycemic clamp. The variation of insulin resistance during puberty in girls may be likely explained by growth hormone=IGF-1 axis changes during puberty (Amiel et al, 1986;Cook et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Waist circumference as a predictor of cardiovascular and metabolic risk factors in obese girls

Maffeis¹,

Corciulo²,

Livieri³

et al. 2003

Eur J Clin Nutr

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Objectives: (a) to explore the relationship between waist circumference and certain cardiovascular risk factors in a group of girls; and (b) to assess the clinical relevance of waist circumference in identifying girls with higher cardiovascular risk across puberty. Subjects and methods: One-hundred and fifty-five overweight or obese girls aged 5 -16 y were recruited. Overweight and obesity were defined on the basis of BMI, according to Cole. Results: Waist circumference was significantly correlated with plasma insulin (r ¼ 0.43; P < 0.001), systolic blood pressure (r ¼ 0.22; P ¼ 0.007) and IR HOMA (r ¼ 0.40; P < 0.001). A multivariate linear correlation analysis showed that, when adjusted for age and Tanner stage, waist circumference was significantly associated with plasma insulin (r 2 ¼ 0.23; P < 0.01), IR HOMA (r 2 ¼ 0.17; P < 0.02), systolic and diastolic blood pressure (r 2 ¼ 0.20; P ¼ 0.006 and r 2 ¼ 0.32; P < 0.001, respectively). A logistic regression analysis, using IR HOMA as the dependent variable, showed that waist circumference was a significant independent risk factor of insulin resistance (IR HOMA 5 2.6) in this group of girls (OR 1.10; 95% CI 1.03 -1.18; P ¼ 0.003), independently of their age and Tanner stage. Conclusions: Waist circumference of these girls was independently associated with certain cardiovascular risk factors, in particular insulin resistance and diastolic blood pressure, independently of age and Tanner stage. Thus suggesting that waist circumference may be reasonably included in clinical practice as a simple tool that may help to identify sub-groups of obese girls at higher metabolic risk across puberty.

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Section: Discussionmentioning

confidence: 99%

Waist circumference as a predictor of cardiovascular and metabolic risk factors in obese girls

Maffeis¹,

Corciulo²,

Livieri³

et al. 2003

Eur J Clin Nutr

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“…Others have also reported that insulin resistance remains elevated throughout puberty. 2,24,39 However, insulin resistance does eventually decrease during adulthood, while the amount of FM and percentage body fat increases, so factors other than FM are probably also involved. Our results that insulin resistance was most related to total adiposity are contrary to adult data that have shown AVF is most strongly linked to insulin resistance in adults.…”

Section: Discussionmentioning

confidence: 99%

Pubertal alterations in growth and body composition. VI. Pubertal insulin resistance: relation to adiposity, body fat distribution and hormone release

et al. 2002

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OBJECTIVE:To investigate the independent influence of alterations in fat mass, body fat distribution and hormone release on pubertal increases in fasting serum insulin concentrations and on insulin resistance assessed by the homeostasis model (HOMA). DESIGN AND SUBJECTS: Cross-sectional investigation of pre-(n ¼ 11, n ¼ 8), mid-(n ¼ 10, n ¼ 11), and late-pubertal (n ¼ 10, n ¼ 11) boys and girls with normal body weight and growth velocity. MEASUREMENTS: Body composition (by a four-compartment model), abdominal fat distribution and mid-thigh interfascicular plus intermuscle (extramyocellular) fat (by magnetic resonance imaging), total body subcutaneous fat (by skinfolds), mean nocturnal growth hormone (GH) release and 06:00 h samples of serum insulin, sex steroids, leptin and insulin-like growth factor-I (IGF-I). RESULTS: Pubertal insulin resistance was suggested by greater (P < 0.001) fasting serum insulin concentrations in the latepubertal than pre-and mid-pubertal groups while serum glucose concentrations were unchanged and greater (P < 0.001) HOMA values in late-pubertal than pre-and mid-pubertal youth. From univariate correlation fat mass was most related to HOMA (r ¼ 0.59, P < 0.001). Two hierarchical regression models were developed to predict HOMA. In one approach, subject differences in sex, pubertal maturation, height and weight were held constant by adding these variables as a block in the first step of the model (r 2 ¼ 0.36). Sequential addition of fat mass (FM) increased r 2 (r 2 (inc)remental ¼ 0.08, r 2 ¼ 0.44, P < 0.05) as did the subsequent addition of a block of fat distribution variables (extramyocellular fat, abdominal visceral fat, and sum of skinfolds; r 2 inc ¼ 0.11, r 2 ¼ 0.55, P < 0.05). Sequential addition of a block of hormone variables (serum IGF-I and log (10) leptin concentrations; r 2 inc ¼ 0.04, P > 0.05) did not reliably improve r 2 beyond the physical characteristic and adiposity variables. In a second model, differences in sex and pubertal maturation were again held constant (r 2 ¼ 0.25), but body size differences were accounted for using percentage fat data. Sequential addition of percentage body fat (r 2 (inc)remental ¼ 0.11, r 2 ¼ 0.36, P < 0.05), then a block of fat distribution variables (percentage extramyocellular fat, percentage abdominal visceral fat, and percentage abdominal subcutaneous fat; r 2 inc ¼ 0.08, r 2 ¼ 0.44, P ¼ 0.058), and then a block of serum IGF-I and log (10) leptin concentrations (r 2 inc ¼ 0.07, r 2 ¼ 0.51, P < 0.05) increased r 2 . Mean nocturnal GH release was not related to HOMA (r ¼ 7 0.04, P ¼ 0.75) and therefore was not included in the hierarchical regression models. CONCLUSION: Increases in insulin resistance at puberty were most related to FM. Accumulation of fat in the abdominal visceral, subcutaneous and muscular compartments may increase insulin resistance at puberty beyond that due to total body fat. Serum concentrations of leptin and IGF-I may further modulate HOMA beyond the effects of adiposity and fat distribution. However, the results...

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“…[1][2][3][4] In Caucasian children, decreased SI during puberty is accompanied by increased insulin secretion that normalizes as insulin resistance improves near the end of puberty. 5 Cross-sectionally, Moran et al 3 showed that SI (measured using the euglycemic-hyperinsulinemic clamp) was highest in Tanner stage I, lowest in Tanner stage III (B20% lower than stage I), and near prepubertal levels in Tanner stage V. Using a longitudinal design, Goran and Gower 2 observed that the pubertal transition from Tanner stage I to III was associated with a 32% reduction in SI (measured by the intravenous glucose tolerance test and minimal modeling) in Caucasian and African-Americans which was consistent across a range of body fatness.…”

Section: Introductionmentioning

confidence: 99%

Insulin sensitivity, insulin secretion and β-cell function during puberty in overweight Hispanic children with a family history of type 2 diabetes

et al. 2005

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OBJECTIVE:To examine cross-sectional differences in insulin sensitivity, insulin secretion and b-cell function during puberty in overweight Hispanic boys and girls with a family history of type 2 diabetes. STUDY DESIGN AND PARTICIPANTS: This cross-sectional, observational study included 214 8-13-y-old Hispanic children with a BMI percentile Z85th percentile and family history of type 2 diabetes. METHODS AND ANALYSES: Participants underwent a physical examination, body composition measures, oral glucose tolerance test (OGTT), and frequently-sampled intravenous glucose tolerance test. Unadjusted and adjusted general linear models (GLM) tested whether insulin/glucose dynamics differed by Tanner stage and gender. RESULTS: Unadjusted group comparisons showed that fasting insulin increased whereas insulin sensitivity (SI) and the disposition index (DI) (a measure of pancreatic b-cell function) decreased across Tanner stage groups (all Po0.05). No differences in the acute insulin response to glucose (AIRg), fasting glucose or 2-h glucose were found. After adjusting for covariates, there was no independent effect of Tanner stage on SI (P ¼ 0.9) or AIRg (P ¼ 0.2), but DI was slightly lower in later Tanner stages suggesting decreased b-cell function in the more mature groups (P ¼ 0.10). CONCLUSIONS: Overweight Hispanic children with a family history of type 2 diabetes may represent a unique population given that pubertal insulin resistance was not evident once analyses controlled for body composition. Longitudinal analyses are required to determine whether the slightly diminished b-cell function in later Tanner stages plays a role in the development of type 2 diabetes.

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Effects of maturational stage on insulin sensitivity during puberty.

Cited by 81 publications

References 0 publications

Waist circumference as a predictor of cardiovascular and metabolic risk factors in obese girls

Waist circumference as a predictor of cardiovascular and metabolic risk factors in obese girls

Pubertal alterations in growth and body composition. VI. Pubertal insulin resistance: relation to adiposity, body fat distribution and hormone release

Insulin sensitivity, insulin secretion and β-cell function during puberty in overweight Hispanic children with a family history of type 2 diabetes

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