Influence of the crosstalk between growth hormone and insulin signalling on the modulation of insulin sensitivity

Dominici, Fernando Pablo; Argentino, Danila P.; Muñoz, Marina Cecilia; Miquet, Johanna G.; Sotelo, Ana I.; Turyn, Daniel

doi:10.1016/j.ghir.2005.07.001

Cited by 140 publications

(129 citation statements)

References 162 publications

(245 reference statements)

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“…Besides changes in adipocytokines (e.g., adiponectin) (47), other mechanisms have been proposed to explain the modulatory effects of GH on insulin (5,48), including upregulation of suppressor of cytokine signaling (SOCS) proteins (e.g., SOCS-3). However, a role for SOCS is still undefined.…”

Section: Discussionmentioning

confidence: 99%

Growth Hormone Regulation of p85α Expression and Phosphoinositide 3-Kinase Activity in Adipose Tissue

et al. 2007

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Phosphoinositide (PI) 3-kinase is involved in insulin-mediated effects on glucose uptake, lipid deposition, and adiponectin secretion from adipocytes. Genetic disruption of the p85␣ regulatory subunit of PI 3-kinase increases insulin sensitivity, whereas elevated p85␣ levels are associated with insulin resistance through PI 3-kinase-dependent and -independent mechanisms. Adipose tissue plays a critical role in the antagonistic effects of growth hormone (GH) on insulin actions on carbohydrate and lipid metabolism through changes in gene transcription. The objective of this study was to assess the role of the p85␣ subunit of PI 3-kinase and PI 3-kinase signaling in GH-mediated insulin resistance in adipose tissue. To do this, p85␣ mRNA and protein expression and insulin receptor substrate (IRS)-1-associated PI 3-kinase activity were measured in white adipose tissue (WAT) of mice with GH excess, deficiency, and sufficiency. Additional studies using 3T3-F442A cells were conducted to confirm direct effects of GH on free p85␣ protein abundance. We found that p85␣ expression 1) is decreased in WAT from mice with isolated GH deficiency, 2) is increased in WAT from mice with chronic GH excess, 3) is acutely upregulated in WAT from GH-deficient and -sufficient mice after GH administration, and 4) is directly upregulated by GH in 3T3-F442A adipocytes. The insulininduced increase in PI 3-kinase activity was robust in mice with GH deficiency, but not in mice with GH excess. In conclusion, GH regulates p85␣ expression and PI 3-kinase activity in WAT and provides a potential explanation for 1) the insulin hypersensitivity and associated obesity and hyperadiponectinemia of GH-deficient mice and 2) the insulin resistance and associated reduced fat mass and hypoadiponectinemia of mice with GH excess. Diabetes

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Section: Discussionmentioning

confidence: 99%

Growth Hormone Regulation of p85α Expression and Phosphoinositide 3-Kinase Activity in Adipose Tissue

et al. 2007

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“…Treatment of acromegalic patients with somatostatin analogs improves insulin resistance (101). Postreceptor crosstalk between the insulin receptor and GH receptor signaling pathways is believed to play a key role in this process (102).…”

Section: Glucose Homeostasismentioning

confidence: 99%

Genetic disorders in the GH–IGF-I axis in mouse and man

Walenkamp

Wit²

2007

eur j endocrinol

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Animal knockout experiments have offered the opportunity to study genes that play a role in growth and development. In the last few years, reports of patients with genetic defects in GH-IGF-I axis have greatly increased our knowledge of genetically determined causes of short stature. We will present the animal data and human reports of genetic disorders in the GH-IGF-I axis in order to describe the role of the GH-IGF-I axis in intrauterine and postnatal growth. In addition, the effects of the GH-IGF-I axis on the development and function of different organ systems such as brain, inner ear, eye, skeleton, glucose homeostasis, gonadal function, and immune system will be discussed. The number of patients with genetic defects in the GH-IGF-I axis is small, and a systematic diagnostic approach and selective genetic analysis in a patient with short stature are essential to identify more patients. Finally, the implications of a genetic defect in the GH-IGF-I axis for the patient and the therapeutic options will be discussed.European Journal of Endocrinology 157 S15-S26

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“…In turn, we can then postulate that growth hormone and insulin can interact directly by signaling "crosstalk" and that insulin regulation of growth hormone signaling is associated with the duration of exposure to insulin. Although evidence suggests that chronic administration of excessive growth hormone can interfere with the activation of specific pathways by insulin [49,50], several other proteins have also been shown to be involved in the mechanisms underlying growth hormone-induced insulin resistance. For example, the results of Xu and Messina [49] and Domenici et al [50] showed that insulin-like growth factor-1 (IGF-1) participates in the control of insulin sensitivity and plays an important role in the hormone balance between growth hormone and insulin.…”

Section: Effects Of Growth Hormone On Dawn Phenomenon In Healthy Adultsmentioning

confidence: 99%

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

Shih¹,

Ho²

2016

J Diabetes Metab

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This review addresses the effects of growth hormone on diurnal insulin sensitivity in normal, patients with type 2 diabetes mellitus (T2DM) and animal models described in our previous studies. Results confirmed the presence of diurnal insulin sensitivity, or greater insulin sensitivity in the morning, in normal subjects. The exact cause of this circadian rhythm in plasma glucose levels in healthy subjects has not been established, and nocturnal surges in growth hormone secretion remain a possible explanation. Results showed that growth hormone is an important factor controlling the diurnal variation of glucose tolerance and insulin sensitivity in rats. Data from our previous study provided direct evidence that the role of growth hormone in regulating insulin sensitivity in healthy subjects may be related to changes in the metabolic clearance rate of insulin and the metabolism of non-esterified fatty acids. A different circadian rhythm for plasma glucose appears to be present in patients with T2DM with nadirs in the early evening and peaks in the early morning, indicating greater insulin sensitivity in the evening. As in normal subjects, the exact cause of these circadian rhythms in the plasma glucose levels of patients with T2DM provided direct evidence that the reduction in insulin sensitivity may be due to the nocturnal surge of growth hormone in the early morning hours.

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Influence of the crosstalk between growth hormone and insulin signalling on the modulation of insulin sensitivity

Cited by 140 publications

References 162 publications

Growth Hormone Regulation of p85α Expression and Phosphoinositide 3-Kinase Activity in Adipose Tissue

Growth Hormone Regulation of p85α Expression and Phosphoinositide 3-Kinase Activity in Adipose Tissue

Genetic disorders in the GH–IGF-I axis in mouse and man

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

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