Relative effects of estrogen, age, and visceral fat on pulsatile growth hormone secretion in healthy women

Veldhuis, Johannes D.; Hudson, S.B.; Erickson, Dana; Bailey, James; Reynolds, G. A.; Bowers, Cyril Y.

doi:10.1152/ajpendo.00230.2009

Cited by 17 publications

(12 citation statements)

References 59 publications

(77 reference statements)

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“…In line with this, impaired GH secretion is reversed following weight loss (Williams et al 1984, Rasmussen et al 1995. Correlative studies assessing the relationship between adiposity and the secretion of GH provide essential information to identify potential factors that suppress GH secretion in obesity (Gill et al 1997, Vahl et al 1997, Veldhuis et al 2009). Recent measures demonstrate that impairments in pulsatile GH secretion in humans precede dietary-induced weight gain (Cornford et al 2011(Cornford et al , 2012 and that the suppression of GH secretion with increased food consumption improves meal tolerance (Cornford et al 2012).…”

Section: Introductionmentioning

confidence: 91%

Increased adiposity and insulin correlates with the progressive suppression of pulsatile GH secretion during weight gain

Steyn

Xie

Huang

et al. 2013

Journal of Endocrinology

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Pathological changes associated with obesity are thought to contribute to GH deficiency. However, recent observations suggest that impaired GH secretion relative to excess calorie consumption contributes to progressive weight gain and thus may contribute to the development of obesity. To clarify this association between adiposity and GH secretion, we investigated the relationship between pulsatile GH secretion and body weight; epididymal fat mass; and circulating levels of leptin, insulin, non-esterified free fatty acids (NEFAs), and glucose. Data were obtained from male mice maintained on a standard or high-fat diet. We confirm the suppression of pulsatile GH secretion following dietary-induced weight gain. Correlation analyses reveal an inverse relationship between measures of pulsatile GH secretion, body weight, and epididymal fat mass. Moreover, we demonstrate an inverse relationship between measures of pulsatile GH secretion and circulating levels of leptin and insulin. The secretion of GH did not change relative to circulating levels of NEFAs or glucose. We conclude that impaired pulsatile GH secretion in the mouse occurs alongside progressive weight gain and thus precedes the development of obesity. Moreover, data illustrate key interactions between GH secretion and circulating levels of insulin and reflect the potential physiological role of GH in modulation of insulin-induced lipogenesis throughout positive energy balance. Key Words" pulsatile GH secretion " dietary-induced weight gain " insulin " non-esterified free fatty acids " adiposity

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Section: Introductionmentioning

confidence: 91%

Increased adiposity and insulin correlates with the progressive suppression of pulsatile GH secretion during weight gain

Steyn

Xie

Huang

et al. 2013

Journal of Endocrinology

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“…Human studies have shown that growth hormone (GH) levels or secretion are altered in visceral obese individuals with a high cardiometabolic risk (85,239,339,373,375,434,577,589,590,613). Many reports suggested that the association between visceral and/or abdominal obesity is independent of total adiposity (85,339,373,434,613).…”

Section: G Growth Hormonementioning

confidence: 99%

Pathophysiology of Human Visceral Obesity: An Update

Tchernof

Després

2013

Physiological Reviews

1,904

1,613

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LTchernof A, Després J-P. Pathophysiology of Human Visceral Obesity: An Update. Physiol Rev 93: 359 -404, 2013; doi:10.1152/physrev.00033.2011.-Excess intra-abdominal adipose tissue accumulation, often termed visceral obesity, is part of a phenotype including dysfunctional subcutaneous adipose tissue expansion and ectopic triglyceride storage closely related to clustering cardiometabolic risk factors. Hypertriglyceridemia; increased free fatty acid availability; adipose tissue release of proinflammatory cytokines; liver insulin resistance and inflammation; increased liver VLDL synthesis and secretion; reduced clearance of triglyceride-rich lipoproteins; presence of small, dense LDL particles; and reduced HDL cholesterol levels are among the many metabolic alterations closely related to this condition. Age, gender, genetics, and ethnicity are broad etiological factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage when facing positive energy balance and weight gain may involve sex hormones, local cortisol production in abdominal adipose tissues, endocannabinoids, growth hormone, and dietary fructose. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity. Thiazolidinediones, estrogen replacement in postmenopausal women, and testosterone replacement in androgen-deficient men have been shown to favorably modulate body fat distribution and cardiometabolic risk to various degrees. However, some of these therapies must now be considered in the context of their serious side effects. Lifestyle interventions leading to weight loss generally induce preferential mobilization of visceral fat. In clinical practice, measuring waist circumference in addition to the body mass index could be helpful for the identification and management of a subgroup of overweight or obese patients at high cardiometabolic risk.

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“…al. were analyzing the effects of a 1 year GH-treatment on adult-onset GHD individuals, in tune with the reports of diminishing GH secretion and action with age69, 70. However, the studies on humans completely contradict in vitro studies as well as in vivo observations in GH- transgenic and deficient rodent models which suggest that GH suppresses adiponectin secretion41, 64, 71, 72.…”

Section: Metabolic Effects Of Gh On the Adipose Tissuementioning

confidence: 99%

Biological effects of growth hormone on carbohydrate and lipid metabolism

Vijayakumar

Novosyadlyy

et al. 2010

Growth Hormone & IGF Research

251

198

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This review will summarize the metabolic effects of growth hormone (GH) on the adipose tissue, liver, and skeletal muscle with focus on lipid and carbohydrate metabolism. The metabolic effects of GH predominantly involve the stimulation of lipolysis in the adipose tissue resulting in an increased flux of free fatty acids (FFAs) into the circulation. In the muscle and liver, GH stimulates triglyceride (TG) uptake ,by enhancing lipoprotein lipase (LPL) expression, and its subsequent storage. The effects of GH on carbohydrate metabolism are more complicated and may be mediated indirectly via the antagonism of insulin action. Furthermore, GH has a net anabolic effect on protein metabolism although the molecular mechanisms of its actions are not completely understood. The major questions that still remain to be answered are (i) What are the molecular mechanisms by which GH regulates substrate metabolism? (ii) Does GH affect substrate metabolism directly or indirectly via IGF-1 or antagonism of insulin action?

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Relative effects of estrogen, age, and visceral fat on pulsatile growth hormone secretion in healthy women

Cited by 17 publications

References 59 publications

Increased adiposity and insulin correlates with the progressive suppression of pulsatile GH secretion during weight gain

Increased adiposity and insulin correlates with the progressive suppression of pulsatile GH secretion during weight gain

Pathophysiology of Human Visceral Obesity: An Update

Biological effects of growth hormone on carbohydrate and lipid metabolism

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