Associations between Bone, Fat Tissue and Metabolic Control in Children and Adolescents with Type 1 Diabetes Mellitus

Wędrychowicz, Anna; Stec, Małgorzata; Sztefko, Krystyna; Starzyk, Jerzy

doi:10.1055/s-0034-1375666

Cited by 24 publications

(29 citation statements)

References 10 publications

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“…This was further reinforced by the lower levels of CTX, a marker of bone resorption, in the T1DM cases. This state of low bone turnover with reduced bone formation in T1DM has been reported previously and has been known to be associated with GH deficiency . To facilitate recruitment, the current study did not stipulate fasting blood samples.…”

Section: Discussionmentioning

confidence: 87%

Deficits in Trabecular Bone Microarchitecture in Young Women With Type 1 Diabetes Mellitus

Abdalrahaman

McComb

Foster

et al. 2015

Journal of Bone and Mineral Research

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The pathophysiological mechanism of increased fractures in young adults with type 1 diabetes mellitus (T1DM) is unclear. We conducted a case-control study of trabecular bone microarchitecture and vertebral marrow adiposity in young women with T1DM. Thirty women with T1DM with a median age (range) age of 22.0 years (16.9, 36.1) attending one outpatient clinic with a median age at diagnosis of 9.7 years (0.46, 14.8) were compared with 28 age-matched healthy women who acted as controls. Measurements included MRI-based assessment of proximal tibial bone volume/total volume (appBV/TV), trabecular separation (appTb.Sp), vertebral bone marrow adiposity (BMA), and abdominal adipose tissue and biochemical markers of GH/IGF-1 axis (IGF-1, IGFBP3, ALS) and bone turnover. Median appBV/TV in cases and controls was 0.3 (0.22, 0.37) and 0.33 (0.26, 0.4), respectively (p ¼ 0.018) and median appTb.Sp in T1DM was 2.59 (2.24, 3.38) and 2.32 (2.03, 2.97), respectively (p ¼ 0.012). The median appBV/TV was 0.28 (0.22, 0.33) in those cases with retinopathy (n ¼ 15) compared with 0.33 (0.25, 0.37) in those without retinopathy (p ¼ 0.02). Although median visceral adipose tissue in cases was higher than in controls at 5733 mm 3 (2030,11,144) and 3460 mm 3 (1808, 6832), respectively (p ¼ 0.012), there was no difference in median BMA, which was 31.1% (9.9, 59.9) and 26.3% (8.5, 49.8) in cases and controls, respectively (p ¼ 0.2). Serum IGF-1 and ALS were also lower in cases, and the latter showed an inverse association to appTbSp (r ¼ -0.30, p ¼ 0.04). Detailed MRI studies in young women with childhood-onset T1DM have shown clear deficits in trabecular microarchitecture of the tibia. Underlying pathophysiological mechanisms may include a microvasculopathy.

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Section: Discussionmentioning

confidence: 87%

Deficits in Trabecular Bone Microarchitecture in Young Women With Type 1 Diabetes Mellitus

Abdalrahaman

McComb

Foster

et al. 2015

Journal of Bone and Mineral Research

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“…By and large, most published clinical studies have reported a correlation between osteocalcin circulating levels and glucose homeostasis in humans as well [29][30][31][32][33][34][35][36][37][38][39][40]. These studies, because of their correlative nature, had to be interpreted cautiously and needed a more direct confirmation; this came once the osteocalcin receptor had been identified.…”

Section: Identification Of Gprc6a As An Osteocalcin Receptor In Mice mentioning

confidence: 99%

An Overview of the Metabolic Functions of Osteocalcin

Wei

Karsenty

2015

Curr Osteoporos Rep

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A recent unexpected development of bone biology is that bone is an endocrine organ regulating a growing number of physiological processes. One of the functions regulated by bone through the hormone osteocalcin is glucose homeostasis. In this overview, we will explain why we hypothesized that bone mass and energy metabolism should be subjected to a coordinated endocrine regulation. We will then review the experiments that revealed the endocrine function of osteocalcin and the cell biology events that allow osteocalcin to become a hormone. We will also illustrate the importance of this regulation to understand whole-body glucose homeostasis in the physiological state and in pathological conditions. Lastly, we will mention epidemiological and genetic evidence demonstrating that this function of osteocalcin is conserved in humans.

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“…The possible contribution of osteocalcin to reduced BMD in T1DM was tested in several studies, mostly using adult patients. In a study of 78 patients aged 11.5±4.3 years with T1DM and 11 controls, serum osteocalcin negatively correlated with HbA1c levels (65). In that study osteocalcin also negatively correlated with leptin, which reflects body adiposity.…”

Section: Introductionmentioning

confidence: 99%

Skeletal growth and bone mineral acquisition in type 1 diabetic children; abnormalities of the GH/IGF-1 axis

Raisingani

Preneet

Kohn

et al. 2017

Growth Hormone & IGF Research

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Type 1 Diabetes Mellitus (T1DM) is one of the most common chronic diseases diagnosed in childhood. Childhood and adolescent years are also the most important period for growth in height and acquisition of skeletal bone mineral density (BMD). The growth hormone (GH)/insulin like growth factor -1 (IGF-1) axis which regulates growth, is affected by T1DM, with studies showing increased GH and decreased IGF-1 levels in children with T1DM. There is conflicting data as to whether adolescents with TIDM are able to achieve their genetically-determined adult height. Furthermore, data support that adolescents with T1DM have decreased peak BMD, although the pathophysiology of which has not been completely defined. Various mechanisms have been proposed for the decrease in BMD including low osteocalcin levels, reflecting decreased bone formation; increased sclerostin, an inhibitor of bone anabolic pathways; and increased leptin, an adipocytokine which affects bone metabolism via central and peripheral mechanisms. Other factors implicated in the increased bone resorption in T1DM include upregulation of the osteoprotegerin/ receptor-activator of the nuclear factor-κB ligand pathway, elevated parathyroid hormone levels, and activation of other cytokines involved in chronic systemic inflammation. In this review, we summarize the clinical studies that address the alterations in the GH/IGF-I axis, linear growth velocity, and BMD in children and adolescents with T1DM; and we review the possible molecular mechanisms that may contribute to an attenuation of linear growth and to the reduction in the acquisition of peak bone mass in the child and adolescent with T1DM.

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Associations between Bone, Fat Tissue and Metabolic Control in Children and Adolescents with Type 1 Diabetes Mellitus

Cited by 24 publications

References 10 publications

Deficits in Trabecular Bone Microarchitecture in Young Women With Type 1 Diabetes Mellitus

Deficits in Trabecular Bone Microarchitecture in Young Women With Type 1 Diabetes Mellitus

An Overview of the Metabolic Functions of Osteocalcin

Skeletal growth and bone mineral acquisition in type 1 diabetic children; abnormalities of the GH/IGF-1 axis

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