Effect of insulin on central catecholamines

Sauter, André; Goldstein, Menek; Engel, Jörgen A.; Ueta, Kento

doi:10.1016/0006-8993(83)90691-1

Cited by 175 publications

(73 citation statements)

References 7 publications

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“…Whereas some authors have found an increase in blood flow in response to local insulin administration [6,7], others have not [8][9][10]. Based on the latter findings it has been concluded that the insulin-induced vasodilatation is centrally mediated [11,12]. In the present study we have carefully investigated the effect of regional hyperinsulinaemia on the putative vasodilatation in the skeletal muscle vascular bed, with special attention to the time course.…”

Section: Introductionmentioning

confidence: 88%

Direct vasodilator effects of physiological hyperinsulin‐aemia in human skeletal muscle

Tack

Schefman

Willems³

et al. 1996

Eur J Clin Investigation

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Abstract. Systemic hyperinsulinaemia induces vasodi latation in human skeletal muscle. This effect is gra dual in onset, and at low insulin levels not maximal until at least 3 h. To investigate whether the vasodi lator response to insulin results from a direct vascular effect, we infused insulin directly into the cannulated brachial artery (perfused forearm technique) in a total of 30 experiments in 20 healthy, lean, normotensive volunteers. Local, intra-arterial, infusion of insulin (180 min, O O m U dL " 1 forearm volumemin" 1, « = 15, forearm venous insulin concentration approximately 540pm olL -1) induced a gradual increase in forearm blood flow (FBF; venous occlusion plethysmography) from 1-86 ± 0*17 to 3*64 ± 0,6 4 m L d L " 1 min~l after 180 min (a n o v a P < 0-001), Percentage increases in FBF after 60, 120 and 180 min averaged 14*4 ± 5-9, 59*4 ± 25*5 and 124*6 ± 51*2% respectively. Fore arm glucose uptake increased from 0*24 ± 0-05 to a maximum of 1*98 ± 0-28 /.¿moldL~l min (P < 0 001). Furthermore, insulin infusion increased forearm lac tate release and potassium uptake. In 10 out of these 15 individuals, the forearm glucose uptake was further increased in a second, separate, repeat experiment with concomitant intra-arterial infusion of glucose 5% (O^mLdL™ 1 m in-1), resulting in forearm venous glucose concentrations of approximately 15 mmol L"*1. This combined infusion achieved a simi lar vasodilator response to the infusion of insulin alone. The individual vascular responses of the two paired experiments showed a strong correlation (r = 0*87, P < 0*01). In five subjects time and vehicle control experiments were performed, showing no changes in FB F or metabolism during the 180 min. W e conclude that the slow vasodilator response to insulin (as observed during systemic infusion) can, at least partly, be explained by a direct vascular effect of insulin. Insulin-mediated skeletal muscle glucose uptake precedes this effect, but seems not to be an im portant determinant of the vasodilator response to insulin.

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Section: Introductionmentioning

confidence: 88%

Direct vasodilator effects of physiological hyperinsulin‐aemia in human skeletal muscle

Tack

Schefman

Willems³

et al. 1996

Eur J Clin Investigation

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“…Consistent with its enriched distribution in adrenergic terminals, insulin is found to promote central catecholaminergic activities by releasing both epinephrine and norepinephrine (20), inhibiting synaptic reuptake of norepinephrine (21), and altering catecholomine kinetics (22). In the hippocampus, insulin is reported to enhance ␣1 adrenergic receptor activity, leading to stimulation of membrane phosphoinositol turnover * The costs of publication of this article were defrayed in part by the payment of page charges.…”

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confidence: 86%

Brain Insulin Receptors and Spatial Memory

Zhao

Hui

et al. 1999

Journal of Biological Chemistry

481

154

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“…Insulin might act at both the hypothalamic and the pituitary level via its multiple metabolic pathways. By binding to speci®c hypothalamic receptors, 89 ± 91 insulin could enhance the release of catecholamines, 92,93 which in turn might stimulate SRIH discharge via b-adrenergic receptors. 94 A direct pituitary effect of insulin is still under debate.…”

Section: Insulinmentioning

confidence: 99%

Growth hormone in obesity

1999

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Growth hormone (GH) secretion, either spontaneous or evoked by provocative stimuli, is markedly blunted in obesity. In fact obese patients display, compared to normal weight subjects, a reduced half-life, frequency of secretory episodes and daily production rate of the hormone. Furthermore, in these patients GH secretion is impaired in response to all traditional pharmacological stimuli acting at the hypothalamus (insulin-induced hypoglycaemia, arginine, galanin, L-dopa, clonidine, acute glucocorticoid administration) and to direct somatotrope stimulation by exogenous growth hormone releasing hormone (GHRH). Compounds thought to inhibit hypothalamic somatostatin (SRIH) release (pyridostigmine, arginine, galanin, atenolol) consistently improve, though do not normalize, the somatotropin response to GHRH in obesity. The synthetic growth hormone releasing peptides (GHRPs) GHRP-6 and hexarelin elicit in obese patients GH responses greater than those evoked by GHRH, but still lower than those observed in lean subjects. The combined administration of GHRH and GHRP-6 represents the most powerful GH releasing stimulus known in obesity, but once again it is less effective in these patients than in lean subjects. As for the peripheral limb of the GH ± insulin-like growth factor I (IGF-I) axis, high free IGF-I, low IGF-binding proteins 1 (IGFBP-1) and 2 (IGFBP-2), normal or high IGFBP-3 and increased GH binding protein (GHBP) circulating levels have been described in obesity. Recent evidence suggests that leptin, the product of adipocyte speci®c ob gene, exerts a stimulating effect on GH release in rodents; should the same hold true in man, the coexistence of high leptin and low GH serum levels in human obesity would ®t in well with the concept of a leptin resistance in this condition. Concerning the in¯uence of metabolic and nutritional factors, an impaired somatotropin response to hypoglycaemia and a failure of glucose load to inhibit spontaneous and stimulated GH release are well documented in obese patients; furthermore, drugs able to block lipolysis and thus to lower serum free fatty acids (NEFA) signi®cantly improve somatotropin secretion in obesity. Caloric restriction and weight loss are followed by the restoration of a normal spontaneous and stimulated GH release. On the whole, hypothalamic, pituitary and peripheral factors appear to be involved in the GH hyposecretion of obesity. A SRIH hypertone, a GHRH de®ciency or a functional failure of the somatotrope have been proposed as contributing factors. A lack of the putative endogenous ligand for GHRP receptors is another challenging hypothesis. On the peripheral side, the elevated plasma levels of NEFA and free IGF-I may play a major role. Whatever the cause, the defect of GH secretion in obesity appears to be of secondary, probably adaptive, nature since it is completely reversed by the normalization of body weight. In spite of this, treatment with biosynthetic GH has been shown to improve the body composition and the metabolic ef®cacy of lean body mass in obese pa...

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Effect of insulin on central catecholamines

Cited by 175 publications

References 7 publications

Direct vasodilator effects of physiological hyperinsulin‐aemia in human skeletal muscle

Direct vasodilator effects of physiological hyperinsulin‐aemia in human skeletal muscle

Brain Insulin Receptors and Spatial Memory

Growth hormone in obesity

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