A comparison of the effects of IGF‐I and insulin on glucose metabolism, fat metabolism and the cardiovascular system in normal human volunteers

Russell-Jones, DL; Bates, Andrew; Umpleby, AM; Hennessy, T. R.; Bowes, S. B.; Hopkins, KD; Jackson, Nicola; Kelly, James; Shojaee‐Moradie, Fariba; Jones, R.H.

doi:10.1111/j.1365-2362.1995.tb01721.x

Cited by 74 publications

(40 citation statements)

References 19 publications

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“…It also caused increases in cardiac output, heart rate and stroke volume. Insulin infusion caused similar results, except for decreased NEFAs and no significant changes in cardiovascular variables [283].…”

Section: Glucose Metabolismsupporting

confidence: 55%

IGF-1 and atherothrombosis: relevance to pathophysiology and therapy

et al. 2011

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IGF-1 (insulin-like growth factor-1) plays a unique role in the cell protection of multiple systems, where its fine-tuned signal transduction helps to preserve tissues from hypoxia, ischaemia and oxidative stress, thus mediating functional homoeostatic adjustments. In contrast, its deprivation results in apoptosis and dysfunction. Many prospective epidemiological surveys have associated low IGF-1 levels with late mortality, MI (myocardial infarction), HF (heart failure) and diabetes. Interventional studies suggest that IGF-1 has anti-atherogenic actions, owing to its multifaceted impact on cardiovascular risk factors and diseases. The metabolic ability of IGF-1 in coupling vasodilation with improved function plays a key role in these actions. The endothelial-protective, anti-platelet and anti-thrombotic activities of IGF-1 exert critical effects in preventing both vascular damage and mechanisms that lead to unstable coronary plaques and syndromes. The pro-survival and anti-inflammatory short-term properties of IGF-1 appear to reduce infarct size and improve LV (left ventricular) remodelling after MI. An immune-modulatory ability, which is able to suppress 'friendly fire' and autoreactivity, is a proposed important additional mechanism explaining the anti-thrombotic and anti-remodelling activities of IGF-1. The concern of cancer risk raised by long-term therapy with IGF-1, however, deserves further study. In the present review, we discuss the large body of published evidence and review data on rhIGF-1 (recombinant human IGF-1) administration in cardiovascular disease and diabetes, with a focus on dosage and safety issues. Perhaps the time has come for the regenerative properties of IGF-1 to be assessed as a new pharmacological tool in cardiovascular medicine.

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Section: Glucose Metabolismsupporting

confidence: 55%

IGF-1 and atherothrombosis: relevance to pathophysiology and therapy

et al. 2011

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“…IGF-I shares structural homology and downstream signaling pathways with insulin, and laboratory data have shown that IGF-I has insulin-like effects on peripheral uptake of glucose and fatty acids [1,10]. Further, exogenous administration of recombinant human IGF-I enhances insulin sensitivity in healthy adults [11,12] as well as those with type 2 diabetes [13]. Insulin resistance states including obesity, a strong risk factor for type 2 diabetes, have been associated with altered levels of IGF-I and its binding proteins in circulation [14].…”

Section: Introductionmentioning

confidence: 99%

The role of insulin‐like growth factor‐I and its binding proteins in glucose homeostasis and type 2 diabetes

Rajpathak

Gunter

Wylie‐Rosett

et al. 2009

Diabetes Metabolism Res

221

163

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Summary This review addresses the possible role of the insulin-like growth factor (IGF)-axis in normal glucose homoeostasis and in the etiopathogenesis of type 2 diabetes. IGF-I, a peptide hormone, shares amino acid sequence homology with insulin and has insulin-like activity; most notably, the promotion of glucose uptake by peripheral tissues. Type 2 diabetes as well as pre-diabetic states, including impaired fasting glucose and impaired glucose tolerance, are associated cross-sectionally with altered circulating levels of IGF-I and its binding proteins (IGFBPs). Administration of recombinant human IGF-I has been reported to improve insulin sensitivity in healthy individuals as well as in patients with insulin resistance and type 2 diabetes. Further, IGF-I may have beneficial effects on systemic inflammation, a risk factor for type 2 diabetes, and on pancreatic β-cell mass and function. There is considerable inter-individual heterogeneity in endogenous levels of IGF-I and its binding proteins; however, the relationship between these variations and the risk of developing type 2 diabetes has not been extensively investigated. Large prospective studies are required to evaluate this association.

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“…It is thought that this occurs both by stimulation of peripheral glucose utilisation [18] and suppression of hepatic glucose production [19][20][21]. The mechanism of this latter effect is unclear as hepatic expression of the IGF-I receptor is low [22].…”

Section: Rhigf-i and Carbohydrate Metabolismmentioning

confidence: 99%