Administration of growth hormone in selectively protein-deprived rats decreases BMD and bone strength

Ammann, Patrick; Brennan, Tara Clare; Mekraldi, Samia; Aubert, Michel L.; Rizzoli, René

doi:10.1016/j.bone.2010.02.015

Cited by 8 publications

(4 citation statements)

References 42 publications

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“…As mentioned above, vitamin D, glucocorticoids, and parathyroid hormone modulate the material properties of bone ECM, at least in part through their effects on bone remodeling. Osteoblast-derived IGF-1, but not systemic growth hormone 83 , is sufficient to protect several aspects of bone quality, including the bone ECM material properties measured by nanoindentation, from the deleterious effects of a low protein diet 84 . Although growth hormone increased the cross-sectional area of cortical bone, this change in bone geometry did not produce the expected increase in macromechanical behavior.…”

Section: Molecular Mechanisms Controlling Bone Qualitymentioning

confidence: 99%

Biological Regulation of Bone Quality

Alliston

2014

Curr Osteoporos Rep

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The ability of bone to resist fracture is determined by the combination of bone mass and bone quality. Like bone mass, bone quality is carefully regulated. Of the many aspects of bone quality, this review focuses on biological mechanisms that control the material quality of the bone extracellular matrix (ECM). Bone ECM quality depends upon ECM composition and organization. Proteins and signaling pathways that affect the mineral or organic constituents of bone ECM impact bone ECM material properties, such as elastic modulus and hardness. These properties are also sensitive to pathways that regulate bone remodeling by osteoblasts, osteoclasts, and osteocytes. Several extracellular proteins, signaling pathways, intracellular effectors, and transcription regulatory networks have been implicated in the control of bone ECM quality. A molecular understanding of these mechanisms will elucidate the biological control of bone quality and suggest new targets for the development of therapies to prevent bone fragility.

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Section: Molecular Mechanisms Controlling Bone Qualitymentioning

confidence: 99%

Biological Regulation of Bone Quality

Alliston

2014

Curr Osteoporos Rep

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“…Some caution should be applied to these findings as the links identified may not indicate a potential to influence milk production through the skeletal axis. Studies in rats (Ammann et al 2010) highlight an interaction between protein intake and bone responses to bovine growth hormone, because rats with low protein intake increased osteoclast surface area, but had lower bone mineral density and strength. The loss of bone mass in humans associated with low protein diets (Ammann et al 2010) may indicate the potential for protein loss in cattle to be a factor in the susceptibility of older cattle to hypocalcemia.…”

Section: Hormonal Interventionmentioning

confidence: 99%

Influencing the future: interactions of skeleton, energy, protein and calcium during late gestation and early lactation

Lean

DeGaris²,

Celi

et al. 2014

Anim. Prod. Sci.

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Marked improvements in milk production, health and reproduction have resulted from manipulations of the pre-calving diet. An understanding of the underlying physiological changes resulting from manipulation of late gestational diets is needed in order to refine and enhance these responses. The physiology of late gestation and early lactation of the dairy cow is examined in the context of exploring the hypothesis that changes in physiology occur not only through homeostatic, but also homeorhetic change. Studies in mice and man have identified a pivotal role for skeleton, particularly through production of active forms of osteocalcin, in integrating energy metabolism. Skeleton appears to particularly influence lipid metabolism and vice versa. Further insights into the factors influencing skeletal function and calcium (Ca) metabolism are emerging, including the potential for negative dietary cation anion difference (DCAD) diets to upregulate the responses of the skeleton in metabolism through increased bone mobilisation and in enhancing responses to parathyroid hormone. The rumen appears to be an important site of absorption of Ca, but physiological mechanisms influencing this uptake are not clear. We provide quantitative evidence of the magnitude of responses that reflect relationships linking Ca metabolism, skeleton and production, using meta-analytic methods. Negative DCAD diets increase milk production in multiparous cattle, but not in heifers. Further, examination of concentrations of metabolites related to energy metabolism obtained from cattle exposed to a negative DCAD diet over calving identified a dominant role for Ca concentrations, which were associated with blood-free fatty acids (NEFA), blood 3-hydroxybutyrate, glucose and cholesterol. These relationships were homeostatic, occurring on the same day, but also homeorhetic with concentrations of Ca and NEFA being significantly associated over 21 days. The findings in cattle are consistent with those in the murine models. However, Ca and the skeleton are not the only significant factors in the transition period influencing future performance as hormonal treatments, metabolic demands and sex of the conceptus, and inflammation and the factors controlling this play a role in future performance. Homeorhetic, longer-term, adaptive responses are critical to achieving orchestrated longer-term adaptive responses to calving and lactation. We consider that the teleological question ‘why would a bone-specific hormone (osteocalcin) regulate energy metabolism?’ is answered by the specific needs for integrated metabolism to address the extreme metabolic demands of lactation in many species.

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“…High levels of insulin and insulin treatment in diabetic patients on the other hand are known to decrease circulating GH (17,18). Several investigations in the past have demonstrated that especially protein intake is crucial for an intact GH/IGF system (19,20), and it is well known that a high protein intake as well as individual amino acids can stimulate GH release in healthy subjects (21,22). Diets high in fat have been shown to inhibit GH secretion, most likely due to stimulation of somatostatin (16).…”

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confidence: 99%

Lack of Dietary Carbohydrates Induces Hepatic Growth Hormone (GH) Resistance in Rats

et al. 2011

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GH is a well established regulator of growth, lipid, and glucose metabolism and therefore important for fuel utilization. However, little is known about the effects of macronutrients on the GH/IGF system. We used low-carbohydrate/high-fat diets (LC-HFD) as a model to study the impact of fat, protein, and carbohydrates on the GH/IGF-axis; 12-wk-old Wistar rats were fed either regular chow, a moderate, protein-matched LC-HFD, or a ketogenic LC-HFD (percentage of fat/protein/carbohydrates: chow, 16.7/19/64.3; LC-HF-1, 78.7/19.1/2.2; LC-HF-2, 92.8/5.5/1.7). After 4 wk, body and tibia length, lean body mass, and fat pad weights were measured. Furthermore, we investigated the effects of LC-HFD on 1) secretion of GH and GH-dependent factors, 2) expression and signaling of components of the GH/IGF system in liver and muscle, and 3) hypothalamic and pituitary regulation of GH release. Serum concentrations of IGF-I, IGF binding protein-1, and IGF binding protein-3 were lower with LC-HF-1 and LC-HF-2 (P < 0.01). Both LC-HFD-reduced hepatic GH receptor mRNA and protein expression, decreased basal levels of total and phosphorylated Janus kinase/signal transducers and activators of transcription signaling proteins and reduced hepatic IGF-I gene expression. Hypothalamic somatostatin expression was reduced only with LC-HF-1, leading to increased pituitary GH secretion, higher IGF-I gene expression, and activation of IGF-dependent signaling pathways in skeletal muscle. In contrast, despite severely reduced IGF-I concentrations, GH secretion did not increase with LC-HF-2 diet. In conclusion, lack of carbohydrates in LC-HFD induces hepatic GH resistance. Furthermore, central feedback mechanisms of the GH/IGF system are impaired with extreme, ketogenic LC-HFD.

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Administration of growth hormone in selectively protein-deprived rats decreases BMD and bone strength

Cited by 8 publications

References 42 publications

Biological Regulation of Bone Quality

Biological Regulation of Bone Quality

Influencing the future: interactions of skeleton, energy, protein and calcium during late gestation and early lactation

Lack of Dietary Carbohydrates Induces Hepatic Growth Hormone (GH) Resistance in Rats

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