Serum interleukin‐6 levels and bone mineral density at the femoral neck in post‐menopausal women with Type 1 diabetes

Rachoń, Dominik; Myśliwska, Jolanta; Suchecka-Rachoń, K; Semetkowska-Jurkiewicz, B.; Zorena, Katarzyna; Łysiak−Szydłowska, Wiesława

doi:10.1046/j.1464-5491.2003.00953.x

Cited by 23 publications

(19 citation statements)

References 22 publications

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“…Theoretically, several mechanisms may be suggested to be responsible for low bone mass in DM, such as insulinopenia (14,15), microangiopathy (16,17) and increased interleukin elevation (18). In turn, the lack of metabolic control may potentially affect also the maintenance of bone mass, interfering not only with the equilibrium of mineral metabolism (19,20), but also with bone remodeling activity (21,22).…”

Section: Discussionmentioning

confidence: 99%

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Cutrim¹,

Pereira²,

Paula³

et al. 2007

Braz J Med Biol Res

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We assessed the effect of chronic hyperglycemia on bone mineral density (BMD) and bone remodeling in patients with type 2 diabetes mellitus. We investigated 42 patients with type 2 diabetes under stable control for at least 1 year, 22 of them with good metabolic control (GMC: mean age = 48.8 ± 1.5 years, 11 females) and 20 with poor metabolic control (PMC: mean age = 50.2 ± 1.2 years, 8 females), and 24 normal control individuals (CG: mean age = 46.5 ± 1.1 years, 14 females). We determined BMD in the femoral neck and at the L2-L4 level (DEXA) and serum levels of glucose, total glycated hemoglobin (HbA 1 ), total and ionic calcium, phosphorus, alkaline phosphatase, follicle-stimulating hormone, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor I (IGFI), osteocalcin, procollagen type I C propeptide, as well as urinary levels of deoxypyridinoline and creatinine. HbA 1 levels were significantly higher in PMC patients (12.5 ± 0.6 vs 7.45 ± 0.2% for GMC and 6.3 ± 0.9% for CG; P < 0.05). There was no difference in 25-OH-D, iPTH or IGFI levels between the three groups. BMD values at L2-L4 (CG = 1.068 ± 0.02 vs GMC = 1.170 ± 0.03 vs PMC = 1.084 ± 0.02 g/cm 2 ) and in the femoral neck (CG = 0.898 ± 0.03 vs GMC = 0.929 ± 0.03 vs PMC = 0.914 ± 0.03 g/cm 2 ) were similar for all groups. PMC presented significantly lower osteocalcin levels than the other two groups, whereas no significant difference in urinary deoxypyridine was observed between groups. The present results demonstrate that hyperglycemia is not associated with increased bone resorption in type 2 diabetes mellitus and that BMD is not altered in type 2 diabetes mellitus.

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Section: Discussionmentioning

confidence: 99%

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Cutrim¹,

Pereira²,

Paula³

et al. 2007

Braz J Med Biol Res

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“…Autoimmune destruction of the pancreatic beta cells by infiltrating immune cells triggers pancreatic and systemic upregulation of inflammatory cytokines in humans [43-45] and in animal models of STZ-induced diabetes [46]; moreover, T1D subjects with poor glycemic control exhibit higher levels of inflammation compared to well-controlled subjects [45]. Inflammatory cytokines that are systemically upregulated in T1D subjects, such as tumor necrosis factor alpha (TNF-α), interleukin 1 (IL-1) and interleukin 6 (IL-6) have been demonstrated to have negative effects on osteoblast proliferation and differentiation in vitro , as well as inhibition of bone healing in vivo [47-50].…”

Section: Effects Of Type 1 Diabetes On Osteoblastsmentioning

confidence: 99%

Effects of Type 1 Diabetes on Osteoblasts, Osteocytes, and Osteoclasts

Kalaitzoglou

Popescu

Bunn

et al. 2016

Curr Osteoporos Rep

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Purpose of review To describe the effects of Type 1 diabetes on bone cells. Recent findings Type 1 diabetes (T1D) is associated with low bone mineral density, increased risk of fractures and poor fracture healing. Its effects on the skeleton were primarily attributed to impaired bone formation, but recent data suggests that bone remodeling and resorption are also compromised. The hyperglycemic and inflammatory environment associated with T1D impacts osteoblasts, osteocytes and osteoclasts. The mechanisms involved are complex; insulinopenia, pro-inflammatory cytokine production and alterations in gene expression are a few of the contributing factors leading to poor osteoblast activity and survival and, therefore, poor bone formation. In addition, the observed sclerostin level increase accompanied by decreased osteocyte number and enhanced osteoclast activity in T1D results in uncoupling of bone remodeling. Summary T1D negatively impacts osteoblasts and osteocytes whereas its effects on osteoclasts are not well characterized, although the limited studies available indicate increased osteoclast activity, favoring bone resorption.

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“…IL-6 also plays a role in diabetes. It has been shown that postmenopausal women with type 1 diabetes present higher serum bioactive IL-6 levels than matched healthy controls [29]. Moreover, IL-6 polymorphism seems to be a genetic susceptibility factor for the progression of diabetic nephropathy [16].…”

Section: Testing the Hypothesismentioning

confidence: 99%

Cardiovascular diabetology in the core of a novel interleukins classification: the bad, the good and the aloof

Fisman

Motro

Tenenbaum

2003

Cardiovasc Diabetol

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Serum interleukin‐6 levels and bone mineral density at the femoral neck in post‐menopausal women with Type 1 diabetes

Abstract: Although our study had a small sample size, we found that post-menopausal women with Type 1 diabetes mellitus present lower bone mass and higher serum bioactive IL-6 levels than matched healthy controls, but we were unable to find a correlation between these two parameters.

Cited by 23 publications

References 22 publications

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Lack of relationship between glycemic control and bone mineral density in type 2 diabetes mellitus

Effects of Type 1 Diabetes on Osteoblasts, Osteocytes, and Osteoclasts

Cardiovascular diabetology in the core of a novel interleukins classification: the bad, the good and the aloof

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