Time course of the response to recombinant growth hormone in acidotic mice

Jandziszak, Karina; Suarez, Carlos J.; Saenger, Paul; Brion, Luc P.

doi:10.1007/s004670000327

Cited by 2 publications

(2 citation statements)

References 20 publications

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“…Thus, metabolic acidosis, if not corrected, may contribute to growth retardation in children with chronic renal failure. It has also been reported that growth-hormone resistance may occur in animals with metabolic acidosis [29]. In order to maximize growth, metabolic acidosis needs to be corrected prior to treatment with growth hormone.…”

Section: Metabolic Acidosismentioning

confidence: 99%

Growth-plate cartilage in chronic renal failure

Sanchez

2009

Pediatr Nephrol

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Bone growth occurs in the growth-plate cartilage located at the ends of long bones. Changes in the architecture, abnormalities in matrix organization, reduction in protein staining and RNA expression of factors involved in cell signaling have been described in the growth-plate cartilage of nephrectomized animals. These changes can lead to a smaller growth plate associated with decrease in chondrocyte proliferation, delayed hypertrophy, and prolonged initiation of mineralization and vascular invasion. As a result, chronic renal failure can result in stunted body growth and skeletal deformities. Multiple etiologic factors can contribute to impaired bone growth in renal failure, including suboptimal nutrition, metabolic acidosis, and secondary hyperparathyroidism. Recent findings have also shown the tight connection between chondro/osteogenesis, hematopoiesis, and immunogenesis.

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Section: Metabolic Acidosismentioning

confidence: 99%

Growth-plate cartilage in chronic renal failure

Sanchez

2009

Pediatr Nephrol

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“…Animals were injected with recombinant human GH (Genotropin, 3 mg/kg body weight, i.p.) [50,51]. One hour after injection, mice were sacrificed and their livers were harvested.…”

Section: Acute Gh Administrationmentioning

confidence: 99%

Role of the GH/IGF-I axis in the growth retardation of weaver mice

Yao

Bethin

Yang

et al. 2007

Endocr

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IGF-I is a well-established anabolic growth factor essential for growth and development. Although the role of the GH/IGF-I axis is established for normal postnatal growth, its functional state in neurodegenerative diseases is not fully characterized. The weaver mutant mouse is a commonly used model for studying hereditary cerebellar ataxia and provides an opportunity to investigate the function of IGF-I in postnatal growth following neurodegeneration. Previously, we reported that weaver mice are growth retarded and their body weights correlate with a decrease in circulating IGF-I levels. Because weaver mice have the same food intake/body weight ratios as their wild type littermates, our observation suggests that an impairment of the GH/IGF-I axis, rather than poor nutrition, likely contributes to their growth retardation. This study further investigated the etiology of reduced circulating IGF-I levels. We found that GH levels in weaver mice were reduced following acute insulin injection, but the hepatic GH receptor transduction pathway signaled normally as evidenced by increased STAT5b phosphorylation and IGF-I mRNA levels in response to acute GH administration. In addition, 2-week GH treatment induced a significant increase in body weight and circulating IGF-I levels in homozygous weaver mice but not in wild type littermates. In summary, a deficiency in the GH/IGF-I axis may be partially responsible for postnatal growth retardation in weaver mutant mice. This deficiency may occur at the level of the pituitary and/or hypothalamus and can be improved with GH administration.

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Time course of the response to recombinant growth hormone in acidotic mice

Cited by 2 publications

References 20 publications

Growth-plate cartilage in chronic renal failure

Growth-plate cartilage in chronic renal failure

Role of the GH/IGF-I axis in the growth retardation of weaver mice

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