Impact of treatment with recombinant human GH and IGF-I on visceral adipose tissue and glucose homeostasis in adults

Yuen, Kevin C.J.

doi:10.1016/j.ghir.2006.03.001

Cited by 23 publications

(19 citation statements)

References 57 publications

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“…Multiple factors are most likely involved, including alterations in insulin sensitivity due to increased free fatty acids resulting from the lipolytic effects of excess GH (‘lipotoxic effect’) [48, 49], postreceptor crosstalk between the insulin receptor and GH receptor signaling pathways [50], decreased expression of the insulin-sensitizing adipocytokines adiponectin and visfatin [51, 52] or the hyperinsulinemia induced by the excess GH that reduces the number of insulin receptors and alters their kinase activity [53]. Moreover, GH has stimulatory effects on insulin directly at the level of the β-cell, but prolonged exposure to excess GH results in β-cell failure followed by decreased insulin secretion and glucose tolerance, a feature resembling the long-term sequelae of altered glucose homeostasis in untreated acromegalic patients [54]. …”

Section: Carbohydrate Metabolismmentioning

confidence: 99%

Human Acid-Labile Subunit Deficiency: Clinical, Endocrine and Metabolic Consequences

et al. 2009

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The majority of insulin-like growth factor (IGF)-I and IGF-II circulate in the serum as a complex with the insulin-like growth factor binding protein (IGFBP)-3 or IGFBP-5, and an acid-labile subunit (ALS). The function of ALS is to prolong the half-life of the IGF-I-IGFBP-3/IGFBP-5 binary complexes. Fourteen different mutations of the human IGFALS gene have been identified in 17 patients, suggesting that ALS deficiency may be prevalent in a subset of patients with extraordinarily low serum levels of IGF-I and IGFBP-3 that remain abnormally low upon growth hormone stimulation. Postnatal growth was clearly affected. Commonly, the height standard deviation score before puberty was between –2 and –3, and approximately 1.4 SD shorter than the midparental height SDS. Pubertal delay was found in 50% of the patients. Circulating IGF-II, IGFBP-1, -2 and -3 levels were reduced, with the greatest reduction observed for IGFBP-3. Insulin insensitivity was a common finding, and some patients presented low bone mineral density. Human ALS deficiency represents a unique condition in which the lack of ALS proteins results in the disruption of the entire IGF circulating system. Despite a profound circulating IGF-I deficiency, there is only a mild impact on postnatal growth. The preserved expression of locally produced IGF-I might be responsible for the preservation of linear growth near normal limits.

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Section: Carbohydrate Metabolismmentioning

confidence: 99%

Human Acid-Labile Subunit Deficiency: Clinical, Endocrine and Metabolic Consequences

et al. 2009

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“…Insulin has predominantly metabolic actions, while IGF-I, as well as metabolic actions, is strongly mitogenic and regulates cellular proliferation and growth. Insulin and IGF-I signaling can induce very similar cascades of postreceptor signaling events (2). IGF-I in blood circulates mainly in complexes with IGF binding proteins (IGFBP), which form a mobile reserve.…”

Section: Introductionmentioning

confidence: 99%

Insulin‐like growth factor I (IGF‐I) as a sensitive biomarker of catabolism in patients with gastrointestinal diseases

Nedić

Malenković

Nikolić

et al. 2007

Clinical Laboratory Analysis

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Gastrointestinal ailments evoke changes in the hypothalamic-pituitary-adrenal (HPA) axis and modulation of hepatic protein synthesis. We examined the catabolic effect of certain primary gastrointestinal diseases and surgery on the concentration of insulin-like growth factor I (IGF-I). Blood samples from patients with gastric cancer (GC), cholecystitis (CC), or inguinal hernia (IH) were taken before and after surgery. The concentrations of IGF-I, IGF binding protein-1 (IGFBP-1), insulin, cortisol, and glucose were determined. In GC patients the concentration of IGF-I was reduced and the concentrations of IGFBP-1 and cortisol were elevated preoperatively; after surgery, IGFBP-1 normalized. In CC patients the concentration of IGF-I was low and the concentration of IGFBP-1 was high before cholecystectomy; after surgery IGFBP-1 returned to normal and the concentration of cortisol increased. In IH patients the concentration of IGF-I was low and the concentrations of IGFBP-1 and cortisol were high before surgery; after laparotomy IGFBP-1 returned to normal. The metabolic changes were present in all analyzed patient groups, regardless of the severity of disease and nutrition. The concentration of IGF-I was reduced before surgery and remained reduced after, recommending IGF-I as a metabolic marker in both pre and postoperative examination of patients.

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“…The IGF axis is also an important regulator of glucose homeostasis. IGF-I can directly stimulate glucose uptake, and low plasma IGF-I predicts poor insulin secretion in children and later development of impaired glucose tolerance in adults (17,57).…”

mentioning

confidence: 99%

Repeated betamethasone treatment of pregnant sheep programs persistent reductions in circulating IGF-I and IGF-binding proteins in progeny

Gatford

Owens

Li³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Impact of treatment with recombinant human GH and IGF-I on visceral adipose tissue and glucose homeostasis in adults

Cited by 23 publications

References 57 publications

Human Acid-Labile Subunit Deficiency: Clinical, Endocrine and Metabolic Consequences

Human Acid-Labile Subunit Deficiency: Clinical, Endocrine and Metabolic Consequences

Insulin‐like growth factor I (IGF‐I) as a sensitive biomarker of catabolism in patients with gastrointestinal diseases

Repeated betamethasone treatment of pregnant sheep programs persistent reductions in circulating IGF-I and IGF-binding proteins in progeny

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