Peptide YY (PYY) levels and bone mineral density (BMD) in women with anorexia nervosa

Utz, Andrea L.; Lawson, Elizabeth A.; Misra, Madhusmita; Mickley, Diane; Gleysteen, Suzanne; Herzog, David B.; Klibanski, Anne; Miller, Karen K.

doi:10.1016/j.bone.2008.03.007

Cited by 105 publications

(69 citation statements)

References 34 publications

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“…PYY has also been shown to play a role in bone homeostasis and may be involved peripherally in the regulation of bone formation through osteoblastic Y1 receptors. Elevated PYY levels have been shown to correlate with diminished BMD in women with anorexia nervosa, a condition that results in significant bone loss [36]. However, analysis of a PYY knockout line found that a lack of PYY led to an osteopenic phenotype with reductions in vertebral cancellous bone mass and bone strength [37].…”

Section: Discussionmentioning

confidence: 99%

Osteoblast specific Y1 receptor deletion enhances bone mass

Lee¹,

Nguyen²,

Enriquez³

et al. 2011

Bone

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Neuropeptide Y, Y1 receptors are found in neuronal as well as bone tissue and Y1 signalling has been implicated in the regulation of bone mass. However, the contribution of Y1 receptors located in these different tissues, particularly that of the bone-specific Y1 receptors, to the regulation of bone homeostasis is unclear. Here we demonstrate that osteoblastspecific Y1 receptor deletion resulted in a marked increase in femoral cancellous bone volume, trabecular thickness and trabecular number. This is the result of elevated osteoblast activity as shown by increased mineral apposition rate and bone formation rate, and is associated with an upregulation in the mRNA expression levels of alkaline phosphatase, osteocalcin and dentin matrix protein-1. Furthermore, osteoblastic Y1 receptor deletion also led to increased mineral apposition rate on both the endocortical and the periosteal surfaces resulting in increased femoral diameter. Together these data demonstrate a direct role for the Y1 receptor on osteoblasts in the regulation of osteoblast activity and bone formation in vivo and suggest that targeting Y1 receptor signalling directly in the bone may have potential therapeutic implications for stimulating bone accrual in diseases such as osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Osteoblast specific Y1 receptor deletion enhances bone mass

Lee¹,

Nguyen²,

Enriquez³

et al. 2011

Bone

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“…Other hormonal alterations that contribute to low bone density and lower levels of bone formation markers include low levels of leptin and insulin, and high levels of PYY [31,35]. In women with AN, mean overnight PYY levels correlated negatively with bone density at multiple skeletal sites, and at the spine PYY was a major determinant of bone density variability [69]. …”

Section: Bone Metabolismmentioning

confidence: 99%

The Neuroendocrine Basis of Anorexia Nervosa and Its Impact on Bone Metabolism

Misra¹,

Klibanski²

2011

Neuroendocrinology

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Anorexia nervosa (AN) is a condition of profound undernutrition associated with alterations in various neuroendocrine axes, many of which contribute to a marked impairment in bone accrual and low bone mineral density. This review focuses on changes in the hypothalamo-pituitary-gonadal axis, the growth hormone insulin-like growth factor-1 axis, and the hypothalamo-pituitary-adrenal axis in AN, as well as alterations in various appetite-regulating hormones. In addition, the review discusses low bone mineral density and altered bone microarchitecture in AN, the pathophysiology underlying impaired bone metabolism, and possible therapeutic strategies to optimize bone health.

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“…After correction for BMI in patients with anorexia nervosa, PYY is negatively correlated with areal and estimated volumetric BMD, and negatively correlated with biochemical markers of bone formation and resorption [104,105]. This seems to contradict the PYY knockout model.…”

Section: Peptide Yymentioning

confidence: 56%

Effects of Feeding on Bone Metabolism

Walsh

Eastell

2009

Clinic Rev Bone Miner Metab

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Bone metabolism responds to long-term energy balance, but is also regulated acutely by feeding. In vitro, animal and human studies have demonstrated complex effects of feeding on bone metabolism, which may be mediated through multiple interacting pathways. The most important mediators of the effects of feeding on bone metabolism are likely to be enteric and pancreatic hormones, such as incretins, amylin, preptin, pancreatic polypeptide, and peptide YY. These mediators may regulate bone turnover by direct effects on bone cells and through central nervous system pathways. Small human studies have been conducted to assess the therapeutic potential of these mediators, and although not all had significant effects, this is promising field for new treatments. Dietary composition may also influence bone metabolism, for example protein intake may exert effects through IGF-1, and acid-base balance may influence osteoclast activity and renal calcium excretion. In conclusion, bone metabolism is regulated by long-term energy balance, acute effects of feeding and dietary composition, and there are likely to be multiple interactions between these processes. Some of the endocrine mediators of feeding and bone metabolism have potential as therapeutic agents.

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Peptide YY (PYY) levels and bone mineral density (BMD) in women with anorexia nervosa

Cited by 105 publications

References 34 publications

Osteoblast specific Y1 receptor deletion enhances bone mass

Osteoblast specific Y1 receptor deletion enhances bone mass

The Neuroendocrine Basis of Anorexia Nervosa and Its Impact on Bone Metabolism

Effects of Feeding on Bone Metabolism

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