OBJECTIVE: To determine longitudinal changes in insulin sensitivity (SI), insulin secretion, and beta-cell function during puberty in white and black youth. STUDY DESIGN: The tolbutamide-modified frequently sampled intravenous glucose tolerance test and minimal modeling were used to measure SI, the acute insulin response to glucose (AIRg), and beta-cell function (disposition index, DI) in white (n = 46) and black (n = 46) children (mean [+/-SD] age at baseline = 10.2 +/- 1.7 years). Growth curve models (including 272 observations) with SI, AIRg, and DI regressed on Tanner stage were run after adjusting for covariates. RESULTS: After adjusting for covariates, growth curve models revealed that SI decreased and subsequently recovered by the end of puberty in whites and blacks (both p < .05), AIRg decreased linearly across Tanner stages in both races (both p < .001), and DI decreased across puberty in blacks (p = .001) but not in whites (p = .2). CONCLUSIONS: White and black youth exhibited transient insulin resistance and diminished AIRg during puberty. The progressive decline in DI among blacks versus whites may reflect a unique effect of puberty on beta-cell compensation in blacks. Future studies are needed to identify whether this difference contributes to the increased risk of type II diabetes in young blacks.
OBJECTIVE: To determine longitudinal changes in insulin sensitivity (SI), insulin secretion, and beta-cell function during puberty in white and black youth. STUDY DESIGN: The tolbutamide-modified frequently sampled intravenous glucose tolerance test and minimal modeling were used to measure SI, the acute insulin response to glucose (AIRg), and beta-cell function (disposition index, DI) in white (n = 46) and black (n = 46) children (mean [+/-SD] age at baseline = 10.2 +/- 1.7 years). Growth curve models (including 272 observations) with SI, AIRg, and DI regressed on Tanner stage were run after adjusting for covariates. RESULTS: After adjusting for covariates, growth curve models revealed that SI decreased and subsequently recovered by the end of puberty in whites and blacks (both p < .05), AIRg decreased linearly across Tanner stages in both races (both p < .001), and DI decreased across puberty in blacks (p = .001) but not in whites (p = .2). CONCLUSIONS: White and black youth exhibited transient insulin resistance and diminished AIRg during puberty. The progressive decline in DI among blacks versus whites may reflect a unique effect of puberty on beta-cell compensation in blacks. Future studies are needed to identify whether this difference contributes to the increased risk of type II diabetes in young blacks.
Authors: Maria E Bleil; Bradley M Appelhans; Melissa D Latham; Michelle A Irving; Steven E Gregorich; Nancy E Adler; Marcelle I Cedars Journal: Nurs Res Date: 2015 May-Jun Impact factor: 2.381
Authors: Kevin R Short; Lauren V Pratt; April M Teague; Chiara Dalla Man; Claudio Cobelli Journal: Pediatr Diabetes Date: 2012-07-23 Impact factor: 4.866
Authors: M J Leal-Witt; M Ramon-Krauel; S Samino; M Llobet; D Cuadras; J C Jimenez-Chillaron; O Yanes; C Lerin Journal: Int J Obes (Lond) Date: 2017-08-17 Impact factor: 5.095
Authors: Maria E Bleil; Susan J Spieker; Steven E Gregorich; Alexis S Thomas; Robert A Hiatt; Bradley M Appelhans; Glenn I Roisman; Cathryn Booth-LaForce Journal: J Pediatr Psychol Date: 2021-01-20
Authors: Connie L Tompkins; William Cefalu; Eric Ravussin; Michael Goran; Arlette Soros; Julia Volaufova; Alfonso Vargas; Melinda S Sothern Journal: Int J Pediatr Obes Date: 2010