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J Bone Miner Res. 2017 Jul;32(7):1537-1545. doi: 10.1002/jbmr.3132.

Insulin Resistance and the IGF-I-Cortical Bone Relationship in Children Ages 9 to 13 Years.

Author information

1
Department of Foods and Nutrition, The University of Georgia, Athens, GA, USA.
2
Department of Pediatrics, Augusta University, Augusta, GA, USA.
3
Department of Human Development and Family Science, The University of Georgia, Athens, GA, USA.
4
Department of Kinesiology, The University of Georgia, Athens, GA, USA.
5
Department of Neuroscience and Regenerative Medicine, Augusta University, Augusta, GA, USA.
6
Department of Cellular Biology and Anatomy, Augusta University, Augusta, GA, USA.
7
Department of Statistics, Purdue University, West Lafayette, IN, USA.
8
Department of Nutrition Science, Purdue University, West Lafayette, IN, USA.
9
Department of Physical Therapy, Indiana University, Indianapolis, IN, USA.
10
Department of Medicine, Indiana University, Indianapolis, IN, USA.

Abstract

IGF-I is a pivotal hormone in pediatric musculoskeletal development. Although recent data suggest that the role of IGF-I in total body lean mass and total body bone mass accrual may be compromised in children with insulin resistance, cortical bone geometric outcomes have not been studied in this context. Therefore, we explored the influence of insulin resistance on the relationship between IGF-I and cortical bone in children. A secondary aim was to examine the influence of insulin resistance on the lean mass-dependent relationship between IGF-I and cortical bone. Children were otherwise healthy, early adolescent black and white boys and girls (ages 9 to 13 years) and were classified as having high (n = 147) or normal (n = 168) insulin resistance based on the homeostasis model assessment of insulin resistance (HOMA-IR). Cortical bone at the tibia diaphysis (66% site) and total body fat-free soft tissue mass (FFST) were measured by peripheral quantitative computed tomography (pQCT) and dual-energy X-ray absorptiometry (DXA), respectively. IGF-I, insulin, and glucose were measured in fasting sera and HOMA-IR was calculated. Children with high HOMA-IR had greater unadjusted IGF-I (p < 0.001). HOMA-IR was a negative predictor of cortical bone mineral content, cortical bone area (Ct.Ar), and polar strength strain index (pSSI; all p ≤ 0.01) after adjusting for race, sex, age, maturation, fat mass, and FFST. IGF-I was a positive predictor of most musculoskeletal endpoints (all p < 0.05) after adjusting for race, sex, age, and maturation. However, these relationships were moderated by HOMA-IR (pInteraction  < 0.05). FFST positively correlated with most cortical bone outcomes (all p < 0.05). Path analyses demonstrated a positive relationship between IGF-I and Ct.Ar via FFST in the total cohort (βIndirect Effect  = 0.321, p < 0.001). However, this relationship was moderated in the children with high (βIndirect Effect  = 0.200, p < 0.001) versus normal (βIndirect Effect  = 0.408, p < 0.001) HOMA-IR. These data implicate insulin resistance as a potential suppressor of IGF-I-dependent cortical bone development, though prospective studies are needed.

KEYWORDS:

BONE QCT/µCT; GH/IGF-I; SKELETAL MUSCLE; pQCT

PMID:
28300329
PMCID:
PMC5489353
DOI:
10.1002/jbmr.3132
[Indexed for MEDLINE]
Free PMC Article

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