Evidence suggesting that insulin-like growth factor-I is necessary for the trophic effects of insulin on cartilage growth in vivo.

Alarid, Elaine T.; Schlechter, Nicole; Russell, Sharon M.; Nicoll, Charles S.

doi:10.1210/endo.130.4.1547741

Cited by 9 publications

(3 citation statements)

References 24 publications

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“…They also postulated that insulin acts directly on chondrocyte maturation without utilizing the secondary pathway of binding to IGF-I receptors. Indeed, in vivo (17) but not in vitro (24), the local production of IGF-I is apparently necessary for the growth-promoting role of insulin. Quarto et al (25) also showed that FGF-2 induces chondrocyte proliferation if associated with insulin.…”

Section: Discussionmentioning

confidence: 99%

“…At low concentrations, insulin increases parameters of growth, metabolism and muscle differentiation in 4-day-old chick embryos (16). Insulin has been shown to have an in vitro stimulatory effect on chondrocyte proliferation and activity and an in vivo effect on growth plate width (17). Also, situations of hypoinsulinemia (insulin-dependent diabetes mellitus) and hyperinsulinemia with or without non-insulin-dependent diabetes considerably alter normal bone physiology (18).…”

Section: Introductionmentioning

confidence: 99%

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Insulin impairs the maturation of chondrocytes in vitro

Torres

Andrade

Fonseca

et al. 2003

Braz J Med Biol Res

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The precise nature of hormones and growth factors directly responsible for cartilage maturation is still largely unclear. Since longitudinal bone growth occurs through endochondral bone formation, excess or deficiency of most hormones and growth factors strongly influences final adult height. The structure and composition of the cartilaginous extracellular matrix have a critical role in regulating the behavior of growth plate chondrocytes. Therefore, the maintenance of the threedimensional cell-matrix interaction is necessary to study the influence of individual signaling molecules on chondrogenesis, cartilage maturation and calcification. To investigate the effects of insulin on both proliferation and induction of hypertrophy in chondrocytes in vitro we used high-density micromass cultures of chick embryonic limb mesenchymal cells. Culture medium was supplemented with 1% FCS + 60 ng/ml (0.01 µM) insulin and cultures were harvested at regular time points for later analysis. Proliferating cell nuclear antigen immunoreactivity was widely detected in insulin-treated cultures and persisted until day 21 and [ 3 H]-thymidine uptake was highest on day 14. While apoptosis increased in control cultures as a function of culture time, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-labeled cells were markedly reduced in the presence of insulin. Type II collagen production, alkaline phosphatase activity and cell size were also lower in insulin-treated cultures. Our results indicate that under the influence of 60 ng/ml insulin, chick chondrocytes maintain their proliferative potential but do not become hypertrophic, suggesting that insulin can affect the regulation of chondrocyte maturation and hypertrophy, possibly through an antiapoptotic effect.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Insulin impairs the maturation of chondrocytes in vitro

Torres

Andrade

Fonseca

et al. 2003

Braz J Med Biol Res

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“…In the animal experimental study evaluating the effect of insulin on the tibial growth epiphysis, it was found that insulin caused an increase in the growth plate width and this effect was increased by increasing the amount of IGF-1 in the environment. 34 In the same study, it was observed that the effect of insulin reached a maximum in a certain dose range and then decreased its effect. With regard to previous studies, it can be assumed that insulin may have a safe dose range and may damage healing tissue concentration-related when the dose is incorrect.…”

Section: Smentioning

confidence: 90%

The Effect of Intraarticular Insulin on Chondral Defect Repair

Yıldız¹,

Erşen

Yener

et al. 2020

CARTILAGE

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Objective The aim of this study is to evaluate the effects of intraarticular insulin on the treatment of chondral defects. Design Twenty-four mature New Zealand rabbits were randomly divided into 3 groups as control (Group 1), microfracture (Group 2), and microfracture and insulin (Group 3). Four-millimeter full-thickness cartilage defects were created to the weight-bearing surface on the medial femoral condyles of each rabbit. In the first group, any additional interventions were not performed. Microfracture was performed on defects in groups 2 and 3. Additionally, 10 IU of insulin glargine was administrated into the knee joints of the third group. Three months after surgery, the knee joints were harvested and cartilage quality was assessed according to Wakitani and ICRS (International Cartilage Repair Society) scores histopathologically. Insulin injections were performed into the knees of 2 additional rabbits without creating a cartilage defect to evaluate the potential adverse effects of insulin on healthy cartilage (Group 4). Results The total ICRS and Wakitani scores of the insulin group were found to be significantly lower than the microfracture group but similar to the control group. No negative effects of insulin on healthy cartilage were detected. Intraarticular insulin after surgery has led to a statistically significant decrease in systemic blood sugar levels whereas the decrease observed after administration to intact tissues was not statistically significant. Conclusions Insulin had a negative influence on the quality of cartilage regeneration and had no effect on healthy cartilage. Intraarticular insulin administration does not cause significant systemic effects in intact tissue.

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Insulin enhances the growth of cartilage in organ and tissue cultures of mouse neonatal mandibular condyle

et al. 1993

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Condylar cartilages were cultured in the form of organ cultures on top of collagen sponges in medium containing 2% fetal calf serum and were treated with 3.5-350 nM insulin for 6 days. Doses of 175 nM of insulin caused a marked increase (+96%) in DNA synthesis and in proteoglycan production (+74%), features that manifested themselves structurally by a 60% increase in overall size of the cultured explants. Using a tissue culture system comprised of cartilage progenitor cells, insulin was found to enhance the differentiation of the progenitor cells so that by 6 days in culture an appreciable nodule of differentiated chondrocytes developed. The latter was surrounded by perichondrial cells whereas the extracellular matrix within the newly formed, insulin-induced, nodule reacted positively for cartilage-specific antigens (type II collagen and bone sialoprotein). It is suggested that insulin induces a direct stimulatory effect on progenitor cell proliferation, cartilage differentiation, and extracellular matrix deposition.

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Evidence suggesting that insulin-like growth factor-I is necessary for the trophic effects of insulin on cartilage growth in vivo.

Cited by 9 publications

References 24 publications

Insulin impairs the maturation of chondrocytes in vitro

Insulin impairs the maturation of chondrocytes in vitro

The Effect of Intraarticular Insulin on Chondral Defect Repair

Insulin enhances the growth of cartilage in organ and tissue cultures of mouse neonatal mandibular condyle

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