The Pathogenetic Role of Cortisol in the Metabolic Syndrome: A Hypothesis

Anagnostis, Panagiotis; Athyros, Vasilios G.; Τζιόμαλος, Κωνσταντίνος; Karagiannis, Asterios; Mikhailidis, Dimitri P.

doi:10.1210/endo.150.7.9998

Cited by 145 publications

(220 citation statements)

References 0 publications

Supporting

Mentioning

190

Contrasting

Unclassified

Order By: Relevance

“…The complications of Cushing's syndrome include central obesity, impaired glucose tolerance, insulin resistance, dyslipidemia, hepatic steatosis and systemic arterial hypertension (Arnaldi et al, 2003a) and eventually the metabolic syndrome (Anagnostis et al, 2009;Arnaldi et al, 2003a). Ghrelin levels are decreased in patients with Cushing's syndrome (Libe et al, 2005;Otto et al, 2004).…”

Section: Ghrelin and Cushing's Syndromementioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

Section: Ghrelin and Cushing's Syndromementioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

“…Research into the interplay between the HPA axis and metabolism suggests that the relationship between these systems is established during the prenatal and early postnatal period (3,10,39,53), and maternal stress experienced by the fetus during gestation has proven developmental and metabolic effects (26,34,37,38). Persistent stress also influences bone function, with chronic elevations of cortisol leading to low bone mineral in humans (12).…”

Section: Discussionmentioning

confidence: 99%

“…Scans were analyzed using the manufacturer's software. Metaphyseal bone was analyzed by contour mode 3, peel mode 2, with an outer threshold of 214 g/cm 3 and an inner threshold of 606 g/cm 3 as described elsewhere (2), and diaphyseal bone was analyzed using cortmode 1 with a threshold of 710 g/cm 3 . The coefficient of variation (CV) for total density ranged from 0.48 to 1.47% at the midtibial diaphysis and from 1.32 to 2.23% at the proximal tibial metaphysis, and the CV for total area ranged from 1.47 to 1.72% at the midtibial diaphysis and from 3.73 to 7.11% at the proximal tibial metaphysis without and with repositioning between scans.…”

Section: Methodsmentioning

confidence: 99%

Short-term voluntary exercise in the rat causes bone modeling without initiating a physiological stress response

Rosa¹,

Firth²,

Blair³

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

research has revealed a neuroendocrine connection between the skeleton and metabolism. Exercise alters both bone modeling and energy balance and may be useful in further developing our understanding of this complex interplay. However, research in this field requires an animal model of exercise that does not cause a physiological stress response in the exercised subjects. In this study, we develop a model of short-term voluntary exercise in the female rat that causes bone modeling without causing stress. Rats were randomly assigned to one of three age-matched groups: control, tower climbing, and squat exercise (rising to an erect bipedal stance). Exercise for 21 days resulted in bone modeling as assessed by peripheral quantitative computed tomography. Fecal corticosterone output was used to assess physiological stress at three time points during the study (preexercise, early exercise, and late in the exercise period). There were no differences in fecal corticosterone levels between groups or time points. This model of voluntary exercise in the rat will be useful for future studies of the influence of exercise on the relationship between skeletal and metabolic health and may be appropriate for investigation of the developmental origins of those effects. computed tomography; corticosterone; exercise; metabolism; stress RECENT ADVANCES IN OUR UNDERSTANDING of the dynamic relationship between body structure and metabolism have revealed a neuroendocrine connection between bone remodeling and energy balance, with both bone and fat acting as endocrine organs (14). The osteoblast-specific protein osteocalcin regulates glucose handling through effects on insulin secretion and sensitivity (33). This action is in turn mediated by the adipokine leptin, which inhibits insulin secretion through direct effects on pancreatic ␤-cells (18) and through inhibition of osteocalcin activity (25). The interplay between bone and metabolism has recently been further elucidated by the discovery that the Forkhead family transcription factor FoxO1, a key regulator of insulin handling in multiple tissues, also acts within the osteoblast to control osteocalcin expression and bioactivity (46).Exercise stimulates modeling of the musculoskeletal system (19, 55, 65), alters metabolism (40), and enhances brain function (17), and thus exercise provides an excellent means of exploring the neuroendocrine connection between bone, fat, and energy balance. The rat model of exercise has been used extensively to study the physiological effects of physical activity using such exercise modalities as swimming (24, 32), running (20,29,41,49,52), jumping (57), tower climbing (43), rising to an erect bipedal stance (11, 64), and weight lifting (62). The effects of exercise on bone have been widely characterized in the rat. Ovariectomized rats undergo changes in bone structure that are nearly identical to those seen in human osteoporosis (28,42), and these animals have proven useful for the study of exercise interventions in osteoporosis treatment (36).In examini...

show abstract

“…This is seen particularly on VAT depots, rather than other AT locations, probably for two reasons: higher expression of GR (Bronnegard et al, 1990) and increased reactivation of circulating cortisone due to high 11 -HSD1 expression and/or activity (Alberti et al, 2007;Simonyte et al, 2009). Diagnostic features of GC excess in Cushing's syndrome overlap many of the MetSyn components suggesting that GCs may contribute to the pathogenesis of both states (Anagnostis et al, 2009;M. Wang, 2011).…”

Section: Wwwintechopencommentioning

confidence: 99%

“…Cortisol and 11 -HSDs have been implicated in hypertension (Anagnostis et al, 2009;Andrews et al, 2003;Campino et al, 2010;Cicala & Mantero, 2010;Edwards et al, 1988;Ferrari, 2010;Franks et al, 2004;Funder et al, 1988;Gathercole & Stewart, 2010;Y. Liu et al, 2008;Malavasi et al, 2010;Millis, 2011;Monder et al, 1989;Morales et al, 2008;Mune et al, 1995;Palermo et al, 2004;Paterson et al, 2004;Quinkler & Stewart, 2003;Raff & Findling, 2003;Stewart et al, 1996;Walker & Andrew, 2006;Walker et al, 1993;Wallerath et al, 1999;White et al, 1997).…”

Section: β-Hsd1 and Hypertensionmentioning

confidence: 99%