Glucagon‐releasing activity of guanidine compounds in mouse pancreatic islets

Marco, José; Calle, C.; Hedo, J A; Villanueva, María Luisa

doi:10.1016/0014-5793(76)80246-3

Cited by 27 publications

(26 citation statements)

References 8 publications

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“…Possibly, the mechanism through which creatine affects glucose metabolism is the stimulation of insulin pancreatic secretion, since, although glucose is the greatest stimulator of insulin secretion, it can also be induced by proteins and amino acids. The role of creatine as stimulator of insulin secretion has been demonstrated in in vitro (18)(19) as well as in vivo studies, confirming the very same alterations (16)(17) . Nevertheless, this long-term insulin hypersecretion may induce also to insulin resistance (20) , which has probably not been previously studied in creatine supplementation.…”

Section: Introductionsupporting

confidence: 59%

“…It has been demonstrated in vitro (18)(19) that creatine affects the metabolism of the carbohydrates when directly stimulates the insulin secretion of isolated pancreatic islets. Such fact was confirmed in vivo (16) in a work studying the creatine supplementation in rats in order to observe the long-term effects in the glucose transportation and storage in the skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

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Resistência à insulina com a suplementação de creatina em animais de experimentação

Costallat¹,

Miglioli²,

Silva³

et al. 2007

Rev Bras Med Esporte

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Introduction and objective:Creatine supplementation has been used in order to improve muscular performance. This substance affects glucose metabolism and stimulates the in vitro as well as the in vivo insulin secretion. Nevertheless, long-term insulin hypersecretion may also induce insulin resistance. The present work analyzed the effects of creatine oral supplementation in order to evaluate the possibility of occurrence of resistance to in vivo insulin. Methods: Forty-eight Wistar rats (24 female/ 24 male) were divided in two groups of 24 (control and study) and subdivided in six groups of eight. They were fed with standard food during four weeks, having water ad libitum. Moreover, the study group received dietetic supplement of creatine (0.4 g creatine for 30 ml of water per rat / day). In the 7 th , 14 th , 21 st and 28 th day of the experiment, 12 rats were anesthetized (sodium thiopental 0.15 mL/ 100 g) after six hour-fasting, being submitted to intravenous insulin tolerance test (0.5 mL of 30% regular human insulin and 70% saline solution). The blood samples were collected from the tail veins of the rats, in the basal, three, six, nine, 12 and 15 minutes after insulin administration times. The glucose measurement was performed through the glucose oxidase method. The study was previously approved by the Research Ethics Committee of CCMB-PUC-SP. Results: The mean of the glucose decrease constant (K ITT ) was calculated through the formula 0.693/ T 1/2 . The study group, when compared with the control group, presented insulin resistance at day 21 (p < 0.0004) and day 28 (p < 0.0001). Conclusion: This study shows that extended creatine supplementation may lead to insulin resistance. Besides that, it should be carefully used in individuals with glucose metabolism disturbances.

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Section: Introductionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Resistência à insulina com a suplementação de creatina em animais de experimentação

Costallat¹,

Miglioli²,

Silva³

et al. 2007

Rev Bras Med Esporte

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“…18 and the present study). This effect has also been observed in the adult man (32,52) and rat (3 1). Since exogenous glucagon increases the rate of gluconeogenic substrate conversion to glucose in newborn rats (18,48), the enhanced release of gluckon produced by cortisol probably contributes to its stimulatorv effects on neonatal ~luconeoeenesis.…”

Section: Li'supporting

confidence: 55%

Influence of Exogenous Cortisol and Triglyceride Feeding on Glucose Homeostasis in the Fasted Newborn Rat

et al. 1978

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SummaryThe effects of cortisol injection (0.2 mg/g body wt) at birth and of triglyceride feeding (20 mg/g body wt) 13 hr after birth have been studied in 16hr-old fasted newborn rats. Cortisol produced a 10% decrease in body weight and in protein concentrations of carcass, hindlimb muscle, and liver. Furthermore, cortisol induced a 60% fall in carcass lipid levels. Cortisol caused a 2-fold increase in fasting blood glucose level. This effect resulted from a stimulation of gluconeogenesis (as shown by the 2-to 3-fold rise in the rate of conversion of labeled lactate or alanine to glucose). Several factors influenced this response: 1) increase in circulating gluconeogenic substrates (lactate, pyruvate, alanine,' proline, and glutamine), 2) increase in plasma glucagon, 3) a small rise in plasma free fatty acids (FFA) arising from the catabolism of endogenous lipids, thereby providing additional energy for the hepatic conversion of gluconeogenic substrates to glucose. A concurrent decrease in.glucose utilization was unlikely since: 1) the rate of glucose disappearance after an ip glucose load was similar in fasted and cortisol-treated newborns, and 2) the rise in plasma insulin occurring after cortisol injection would ordinarily tend to increase glucose utilization.Triglyceride feeding was associated with a Zfold rise in fasting blood glucose. This effect was secondary to a stimulation of gluconeogenesis by provision of free FFA, as demonstrated by the 2.5-fold increase in the conversion in vivo of labeled lactate and alanine into glucose.In newborn rats injected with cortisol, the levels of both plasma FFA and blood ketone bodies remained far below those in suckling newborns of the same age. The combination of cortisol injection at birth with triglyceride feeding 13 hr after birth caused a Sfold increase in blood glucose levels in the ldhr-old newborn rats. The stimulating effects of cortisol on gluconeogenesis were potentiated by triglyceride feeding, as shown by the 3-to 4-fold increase in the rate of lactate or alanine conversion to glucose. However, cortisol markedly decreased the ketosis induced by triglyceride feeding and increased plasma triglycerides. SpeculationCorticosteroids have been used in the treatment of symptomatic hypoglycemia in newborn infants. In fasted newborn rats, cortisol partially prevents hypoglycemia, but at the cost of increased protein catabolism. Moreover, cortisol has an antiketogenic effect, thus decreasing the availability of ketones as alternate fuel for brain metabolism and as Drecursor for brain l i~i d svnthesis. If such data can be extrapolated to the human newborn, the prolonged use of corticosteroids in the treatment of neonatal hypoglycemia seems less physiologic than adequate parenteral energy substrate provision in the form of intralipid and gluconeogenic precursors (lactate, amino acids, and glycerol).Profound hypoglycemia has been shown to occur in newborn rats after a fast of 16-24 hr beginning at birth (5,17,19). This hypoglycemia resulted from an inadequate rate of g...

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“…This could either be related to improved pancreatic insulin secretion or to increased peripheral insulin sensitivity. There is a single study to suggest that creatine supplementation might stimulate pancreatic insulin release (17). Indeed, supraphysiological concentrations of guanidinoacetate compounds have been found in vitro to stimulate pancreatic insulin release (1).…”

Section: Discussionmentioning

confidence: 99%

Combined creatine and protein supplementation in conjunction with resistance training promotes muscle GLUT-4 content and glucose tolerance in humans

Derave

Eijnde

Verbessem

et al. 2003

Journal of Applied Physiology

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Glucagon‐releasing activity of guanidine compounds in mouse pancreatic islets

Cited by 27 publications

References 8 publications

Resistência à insulina com a suplementação de creatina em animais de experimentação

Resistência à insulina com a suplementação de creatina em animais de experimentação

Influence of Exogenous Cortisol and Triglyceride Feeding on Glucose Homeostasis in the Fasted Newborn Rat

Combined creatine and protein supplementation in conjunction with resistance training promotes muscle GLUT-4 content and glucose tolerance in humans

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