Cardiovascular and metabolic effects of insulin-like growth factor I at rest and during exercise in humans.

Donath, Marc Y.; Jenni, Rolf; Brunner, Hanspeter; Anrig, M; Kohli, Simi; Glatz, Y; Froesch, E. R.

doi:10.1210/jcem.81.11.8923865

Cited by 31 publications

(13 citation statements)

References 35 publications

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“…In humans, the acute intravenous infusion or subcutaneous administration of recombinant IGF‐I to healthy subjects has been reported to increase cardiac performance, as assessed by impedance cardiography or echocardiography (Russell‐Jones et al ., 1995; Donath et al ., 1996). Systemic side‐effects with metabolic changes were induced by the intravenous infusion of 60 µg/kg of IGF‐I over 3 h (Russell‐Jones et al ., 1995), but not when the same dose was given subcutaneously (Donath et al ., 1996). In this study, glucose levels were unchanged while insulin levels and the GH response to physical exercise were inhibited (Donath et al ., 1996).…”

Section: Effect Of Gh On the Heart: The Experimental Basismentioning

confidence: 99%

“…Systemic side‐effects with metabolic changes were induced by the intravenous infusion of 60 µg/kg of IGF‐I over 3 h (Russell‐Jones et al ., 1995), but not when the same dose was given subcutaneously (Donath et al ., 1996). In this study, glucose levels were unchanged while insulin levels and the GH response to physical exercise were inhibited (Donath et al ., 1996). Moreover, subcutaneous injection of 20 µg/kg of IGF‐I was demonstrated to enhance cardiac inotropism in healthy subjects (Bisi et al ., 1999a).…”

Section: Effect Of Gh On the Heart: The Experimental Basismentioning

confidence: 99%

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Growth hormone and the heart

Colao

Marzullo

Somma

et al. 2001

Clinical Endocrinology

351

296

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Impaired cardiovascular function has recently been demonstrated to potentially reduce life expectancy both in GH deficiency and excess. Experimental and clinical studies have supported the evidence that GH and IGF-I are implicated in cardiac development. In most patients with acromegaly a specific cardiomyopathy, characterized by myocardial hypertrophy with interstitial fibrosis, lympho-mononuclear infiltration and areas of monocyte necrosis, results in biventricular concentric hypertrophy. In contrast, patients with childhood or adulthood-onset GH deficiency (GHD) may suffer both from structural cardiac abnormalities, such as narrowing of cardiac walls, and functional impairment, that combine to reduce diastolic filling and impair left ventricular response to peak exercise. In addition, GHD patients may have an increase in vascular intima-media thickness and a higher occurrence of atheromatous plaques, that can further aggravate the haemodynamic conditions and contribute to increased cardiovascular and cerebrovascular risk. However, several lines of evidence have suggested that the cardiovascular abnormalities can be partially reversed by suppressing GH and IGF-I levels in acromegaly or after GH replacement therapy in GHD patients. Recently, much attention has been focussed on the ability of GH to increase cardiac mass suggesting its possible use in the treatment of chronic nonendocrine heart failure. In fact, GH administration can induce an improvement in haemodynamic and clinical status in some patients. Although these data need to be confirmed in more extensive studies, such promising results seem to open new perspectives for GH treatment in humans.

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Section: Effect Of Gh On the Heart: The Experimental Basismentioning

confidence: 99%

Section: Effect Of Gh On the Heart: The Experimental Basismentioning

confidence: 99%

Growth hormone and the heart

Colao

Marzullo

Somma

et al. 2001

Clinical Endocrinology

351

296

View full text Add to dashboard Cite

show abstract

“…IGF-I administration leads to a decline in circulating levels of GH in young men (28), adolescents with insulin-dependent diabetes (35), and patients with Laron syndrome (36). IGF-I administration leads to a decline in circulating levels of GH in young men (28), adolescents with insulin-dependent diabetes (35), and patients with Laron syndrome (36).…”

Section: Efficacy Of Igf-imentioning

confidence: 99%

One Year of Insulin-Like Growth Factor I Treatment Does Not Affect Bone Density, Body Composition, or Psychological Measures in Postmenopausal Women1

Friedlander

Butterfield

Moynihan

et al. 2001

The Journal of Clinical Endocrinology &Amp; Metabolism

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The activity of the hypothalamic-GH-insulin-like growth factor I (hypothalamic-GH-IGF-I) axis declines with age, and some of the catabolic changes of aging have been attributed to the somatopause. The purpose of this investigation was to determine the impact of 1 yr of IGF-I hormone replacement therapy on body composition, bone density, and psychological parameters in healthy, nonobese, postmenopausal women over 60 yr of age. Subjects (n = 16, 70.6 +/- 2.0 yr, 71.8 +/- 2.8 kg) were randomly assigned to either the self-injection IGF-I (15 microg/kg twice daily) or placebo group and were studied at baseline, at 6 months, and at 1 yr of treatment. There were no significant differences between the IGF-I and placebo groups in any of the measured variables at baseline. Fasting blood IGF-I levels were significantly elevated above baseline values (65.6 +/- 11.9 ng/mL) at 6 months (330.0 +/- 52.8) and 12 months (297.7 +/- 40.8) in the IGF-I treated group but did not change in the placebo subjects. Circulating levels of IGF-binding protein-1 and -3 were unaffected by the IGF-I treatment. Bone mineral density of the forearm, lumbar spine, hip, and whole body [as measured by dual-energy x-ray absorptiometry (DXA)] did not change in either group. Similarly, there was no difference in DXA-measured lean mass, fat mass, or percent body fat throughout the treatment intervention. Muscle strength values (grip, bench press, leg press), blood lipid parameters (cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides), and measures of postmeal glucose disposal were not altered by IGF-I treatment, although postmeal insulin levels were lower in the IGF-I subjects at 12 months. IGF-I did not affect bone turnover markers (osteocalcin and type I collagen N-teleopeptide), but subjects who were taking estrogen had significantly lower turnover markers than subjects who were not on estrogen at baseline, 6 months, and 12 months. Finally, the psychological measures of mood and memory were also not altered by the intervention. Despite the initial intent to recruit additional subjects, the study was discontinued after 16 subjects completed the protocol, because the preliminary analyses above indicated that no changes were occurring in any outcome variables, regardless of treatment regimen. Therefore, we conclude that 1 yr of IGF-I treatment, at a dose sufficient to elevate circulating IGF-I to young normal values, is not an effective means to alter body composition or blood parameters nor improve bone density, strength, mood, or memory in older women.

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“…Donath et al injected IGF-1 subcutaneously (60 Jlg!k:g) in healthy male volunteers and investigated cardiac function and performance by Doppler echocardiography after 2-4 h (62). IGF-1 significantly increased stroke volume, cardiac output, and the ejection fraction.…”

Section: Eugl Ycemic Clamp Studies and Short Infusionsmentioning

confidence: 99%

Metabolic Effects of IGFs

Zapf¹,

Froesch²,

Schmid³

1999

The IGF System

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The relationship between insulin-like growth factors (IGFs) and insulin has been known since the discovery of nonsuppressible insulin-like activity (NSILA) in serum at the beginning of the 1960s ( 1 ), and was derived from the similarities of their biological actions. In the mid-1970s it was found that NSILA consisted of two polypeptides termed IGF-I and IGF-II. They turned out to be not only biologically but also structurally closely related to insulin (2,3). This finding was at first surprising, because the discovery of NSILA had been based on a most prominent feature that essentially distinguished it from insulin: its complete lack of cross-reactivity with insulin antibodies. However, after the elucidation of the primary and tertiary structures ofiGF-I and-II (2-4 ), the reason for this lack of cross-reactivity became apparent (Fig. 1). Insulin contains two main antibody binding sites. One of them comprises the amino (N)-terminal region of the B chain (B2, B3, and B4) plus an adjacent region of the A chain (A8, A9, and AlO). This region is completely different in the IGFs. The second antibody binding site of insulin comprises residues A1 and A19-A21 and the carboxyl (C)-terminal region of the B chain, but this region is covered in the IGFs by the C domain and by a C-terminal extension called the D domain.Despite this distinct immunological difference, IGFs and insulin are close relatives: they not only share important similarities in their structure, their receptors, and their signaling pathways which determine their biological actions, but they also have a common From: Contemporary Endocrinology: The IGF System

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Cardiovascular and metabolic effects of insulin-like growth factor I at rest and during exercise in humans.

Cited by 31 publications

References 35 publications

Growth hormone and the heart

Growth hormone and the heart

One Year of Insulin-Like Growth Factor I Treatment Does Not Affect Bone Density, Body Composition, or Psychological Measures in Postmenopausal Women1

Metabolic Effects of IGFs

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