Calcium homeostasis in chronic streptozotocin-induced diabetes mellitus in the rat

Hough, Stephen; Russell, Jeffrey Burton; Teitelbaum, Steven L.; Avioli, Louis V.

doi:10.1152/ajpendo.1982.242.6.e451

Cited by 47 publications

(35 citation statements)

References 33 publications

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“…Employing short-term (2-week) animal models of streptozotocin diabetes, the low BMD observed in insulinopenic diabetes was earlier explained by secondary hyperparathyroidism and increased bone resorption resulting from a negative calcium balance (impaired intestinal calcium absorption; hypercalciuria) (69,70). Using more appropriate animal models of chronic diabetes (8-10 weeks), and employing time-spaced tetracycline labelled bone histomorphometry, bone formation and resorption were found to be markedly suppressed (71,72,73,74).…”

Section: Bone Turnovermentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

Hough

Pierroz²,

Cooper

et al. 2016

European Journal of Endocrinology

129

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Subjects with type 1 diabetes mellitus (T1DM) have decreased bone mineral density and an up to sixfold increase in fracture risk. Yet bone fragility is not commonly regarded as another unique complication of diabetes. Both animals with experimentally induced insulin deficiency syndromes and patients with T1DM have impaired osteoblastic bone formation, with or without increased bone resorption. Insulin/IGF1 deficiency appears to be a major pathogenetic mechanism involved, along with glucose toxicity, marrow adiposity, inflammation, adipokine and other metabolic alterations that may all play a role on altering bone turnover. In turn, increasing physical activity in children with diabetes as well as good glycaemic control appears to provide some improvement of bone parameters, although robust clinical studies are still lacking. In this context, the role of osteoporosis drugs remains unknown.

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Section: Bone Turnovermentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

Hough

Pierroz²,

Cooper

et al. 2016

European Journal of Endocrinology

129

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show abstract

“…disease on bone (1,2, 7,14,15,21,26,31,33,39,45) as well as the mechanisms by which it affects skeletal tissue and calcium homeostasis (10,19,22,29,36,38). Levin et al (21) suggested that the skeletal effects of diabetes are part of the underlying systemic condition, since they occur early and are unrelated to either the presence or absence of insulin dependence, or to disease duration.…”

mentioning

confidence: 99%

The mineral and mechanical properties of bone in chronic experimental diabetes

Einhorn

Boskey

Gundberg

et al. 1988

Journal Orthopaedic Research

126

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The long-term effects of experimentally induced diabetes on bone were studied in eight male Lewis rats, intravenously (i.v.) injected with 65 mg/kg of streptozocin (STZ) and maintained for 12 months. Eight untreated age-matched rats served as controls. In the STZ-treated rats, experimentally induced diabetes was documented by the presence of hyperglycemia at 24 h and at 3 and 12 months. Significantly less weight was gained and less growth occurred in the STZ-treated rats despite careful attention to feeding and hydration. Mineral alterations were detected in the bones of the animals with experimental diabetes. Decreased hydroxyapatite crystal perfection, decreased Ca/P of the ash, and decreased ash content in the tibial metaphyses with increased ash content in the tibial diaphyses, was noted relative to controls. Bone osteocalcin content was increased in the metaphyses of the STZ-treated rats. While absolute measures of stiffness, torsional strength and energy absorption were decreased in the bones of the STZ-treated animals, when torsional strength and stiffness were normalized for differences in both growth and geometry, the normalized stiffness values for the diabetic bones were increased. The results suggest that in experimental diabetes certain aspects of bone mineralization are adversely affected and lead to reduced strength-related properties. However, a compensatory increase in stiffness occurs. The reason for this increase, although not known, may be related to changes in bone crystal structure.

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“…A dysfunction of the calcium metabolism has been reported to occur in untreated insulin-dependent diabetes mellitus [3]. The basal levels of cytosolic calcium - [Ca 2+ ] i -of renal proximal tubular cells (PTCs) of rats with streptozotocin-induced diabetes are elevated [4].…”

Section: Introductionmentioning

confidence: 99%

High Glucose Levels Alter Angiotensin II-Induced Ca<sup>2+</sup> Uptake via PKC and cAMP Pathways in Renal Proximal Tubular Cells

Park

Shin

Han

2001

Kidney Blood Press Res

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Although a dysfunction of the calcium metabolism occurs in diabetes mellitus, alterations of Ca²⁺ uptake induced by angiotensin II (ANG II) in renal proximal tubular cells (PTCs) grown in high-glucose medium are not fully elucidated. Thus, we examined whether high glucose concentrations can induce an alteration of the ANG II effect on the Ca²⁺ uptake and its action mechanism in primary cultured renal PTCs. PTCs were exposed to different glucose concentrations (5–100 mM) and time intervals (0–48 h). There was a sustained increase of Ca²⁺ uptake at glucose concentrations >15 mM. Thus, we selected 25 mM glucose and incubation for 48 h to maintain a hyperglycemic condition in vitro, unlike short-time regulatin. ANG II significantly inhibited the Ca²⁺ uptake in a dose-dependent manner in a 5-mM glucose medium. In addition, downregulation of ANG II receptors appeared in a glucose dose dependent manner. However, PTCs treated with 25 mM glucose for 48 h, not 12 h, did not exhibit the inhibitory effect of ANG II (10^–7 M) on Ca²⁺ uptake, although the inhibitory effect of ANG II on Ca²⁺ uptake occurred in the presence of 25 mM mannitol or L-glucose. Staurosporine, bisindolylmaleimide I (protein kinase C, PKC, inhibitors), 12-o-tetradecanoylphorbol 13-acetate pretreatment, SQ 22536 (an adenylate cyclase inhibitor), and myristoylated protein kinase A inhibitor amide 14–22 (a protein kinase A inhibitor) blocked the 25-mM-glucose-induced alteration of ANG II effect on Ca²⁺ uptake. These results suggest that both PKC and cyclic adenosine monophosphate (cAMP) pathways are involved in the high-glucose-induced alteration of ANG II effect on Ca²⁺ uptake. Indeed, 25 mM glucose increased PKC activity and cAMP contents. In conclusion, a high glucose concentration altered ANG II induced inhibition of Ca²⁺ uptake via PKC and cAMP pathways in the PTCs.

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Calcium homeostasis in chronic streptozotocin-induced diabetes mellitus in the rat

Cited by 47 publications

References 33 publications

MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

The mineral and mechanical properties of bone in chronic experimental diabetes

High Glucose Levels Alter Angiotensin II-Induced Ca<sup>2+</sup> Uptake via PKC and cAMP Pathways in Renal Proximal Tubular Cells

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