Effects of norepinephrine infusion on in vivo insulin sensitivity and responsiveness

Lupien, J.; Hirshman, Michael F.; Horton, Edward S.

doi:10.1152/ajpendo.1990.259.2.e210

Cited by 26 publications

(23 citation statements)

References 19 publications

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“…One possible explanation for the difference in the glucose utilization responses may be related to differential impact of chronic compared to acute exposure to high catecholamine levels. There are studies in the literature which demonstrate that chronic elevation of norepinephrine [34] or epinephrine [35] improved the whole body glucose disposal as well as the insulin-stimulated glucose uptake in skeletal muscle. Despite the lack of knowledge concerning the mechanism by which chronic high catecholamine levels potentiate whole body glucose disposal, it is recognized that they play a crucial role in the improvement of glucose uptake by rat peripheral tissues after physical training [36], cold exposure [37] or ventromedial hypothalamic stimulation [38].…”

Section: Discussionmentioning

confidence: 99%

Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

León–Quinto¹,

Adnot²,

Portha

1997

Diabetologia

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Section: Discussionmentioning

confidence: 99%

Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

León–Quinto¹,

Adnot²,

Portha

1997

Diabetologia

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“…Epinephrine doses were similar for obese and lean children, and were calculated to induce lipolysis while minimally stimulating the cardiovascular system, according to previous studies in adult men (19)(20)(21). According to the Micromedex Pharmacological Data Base, pediatric doses of epinephrine are 0.020-1.50 g/kg/min.…”

Section: Methodsmentioning

confidence: 99%

In vivo resistance of lipolysis to epinephrine. A new feature of childhood onset obesity.

Bougnères¹,

Stunff²,

Pecqueur³

et al. 1997

J. Clin. Invest.

116

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A decreased mobilization of triglycerides may contribute to fat accumulation in adipocytes, leading to obesity. However, this hypothesis remains to be proven. In this study, epinephrine-induced lipid mobilization was investigated in vivo in nine markedly obese children (160 Ϯ 5% ideal body weight) aged 12.1 Ϯ 0.1 yr during the dynamic phase of fat deposition, compared with six age-matched nonobese children. As an in vivo index of lipolysis, we measured glycerol flux using a nonradioactive tracer dilution approach, and plasma free fatty acid concentrations. In the basal state, the obese children had a 30% lower rate of glycerol release per unit fat mass than the lean children. To study the regulation of lipolysis, epinephrine was infused stepwise at fixed doses of 0.75 and then 1.50 g/min in both groups. In lean children, glycerol flux and plasma free fatty acid increased to an average of 249-246% of basal values, respectively, in response to a mean plasma epinephrine of 396 Ϯ 41 pg/ml. The corresponding increase was only 55-72% in the obese children, although their mean plasma epinephrine reached 606 Ϯ 68 pg/ml. All obese and nonobese children, except an Arg64Trp heterozygote, were homozygotes for Trp at position 64 of their beta 3 -adrenoreceptor. The resistance of lipolysis to epinephrine showed no relationship with the Arg64 polymorphism of the beta 3 -adrenoreceptor gene.In summary, in vivo lipolysis, which mostly reflects the mobilization of lipid stores from subcutaneous adipose tissue, shows a decreased sensitivity to epinephrine in childhood onset obesity. Since our study was carried out in obese children during the dynamic phase of fat accumulation, the observed resistance to catecholamines might possibly be causative rather than the result of obesity. ( J. Clin. Invest. 1997. 99:2568-2573.)

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“…In particular, the dose dependency of glucose [11] or arginine [6,8,12]-stimulated insulin release, biphasic insulin release [11,13], somatostatin inhibition of glucose-induced insulin release [14,15] and insulin desensitization [16,17] were investigated. Several inconsistent data were published as well on the cysteamine depletion of somatostatin from the D cells of the pancreatic islets [18], the pulsatile nature of the insulin secretion [19,20] as well as on the effects of acetylcholine [15,[21][22][23][24][25], dopamine [26], norepinephrine [21,[27][28][29][30][31][32][33][34] and GABA [35] on the insulin secretion. Some of these discrepancies stem from neglected differences in the experimental setup.…”

mentioning

confidence: 99%

Dynamic insulin secretion from perifused rat pancreatic islets

Csernus

Hammer

Peschke

et al. 1998

Cellular and Molecular Life Sciences (CMLS)

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Insulin secretion from isolated pancreatic islets of 8- to 12-day-old rats was investigated in a dynamic in vitro (perifusion) system. The aims of the study were (i) to describe a carefully controlled in vitro method to study the mechanism of insulin secretion and to analyse the effects and dynamic interactions of bioactive compounds on isolated rat pancreatic islets, (ii) to validate the method by comparing fundamental data on the functions of the islets obtained with this method to those collected with other techniques; and (iii) to find novel features of the control of insulin secretion. The method was carefully designed to maintain the functional capacity of the explanted cells. A functional standardization system was elaborated consisting of (i) analysis of the changes in the basal hormone secretion of the cells; (ii) evaluating responses to a standard, specific stimuli (50 mM glucose for 3 min); (iii) determining the alteration of the momentary size of the hormone pool with responses to KCl; and (iv) direct determination of the total intracellular hormone content from the extract of the column. The technique provides accurate quantitative data on the dynamic responses to biologically active compounds that act directly on the pancreatic islets. The islets maintained their full responsiveness for up to 7 days, and responses as close as in 1-min intervals could be distinguished. A linear dose-response relationship was found on the glucose-induced insulin release in case of 3-min stimulation with 4 and 500 mM of glucose (lin-log graph). Utilizing this method, we showed that no desensitization to glucose-induced insulin release can be observed if the responsiveness of the cells is properly maintained and the parameters of the stimulation are carefully designed. Exposure of the explanted islets to 10 microM acetylcholine or 30 mM arginine (Arg) induced a transitory elevation of insulin release similar in shape to that experienced after glucose stimulation. Norepinephrine (NE), dopamine (DA) and somatostatin (SS) did not induce any detectable alteration on the basal insulin secretion of the islets. However, 100 nM SS given together with 50 mM glucose, 30 mM Arg or 10 microM acetylcholine significantly reduced the insulin-releasing effect of these substances (by 75.5, 71.5 and 72.5%, respectively). At the same time, SS did not alter the insulin response of the islets to 100 mM elevation of K+ concentration. SS also inhibited glucose-induced insulin release in a dose-dependent way (ED50 = 22 nM). A similar dose-dependent inhibitory effect on glucose-induced insulin release was found with NE (ED50 = 89 nM) and DA (ED50 = 2.2 microM). gamma-Aminobutyric acid (GABA) did not influence insulin release under similar circumstances.

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Effects of norepinephrine infusion on in vivo insulin sensitivity and responsiveness

Cited by 26 publications

References 19 publications

Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

In vivo resistance of lipolysis to epinephrine. A new feature of childhood onset obesity.

Dynamic insulin secretion from perifused rat pancreatic islets

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