Effects of Priming with D-Glucose on Insulin Secretion from Rat Pancreatic Islets: Increased Responsiveness to Other Secretagogues*

Grill, Valdemar; Rundfeldt, M.

doi:10.1210/endo-105-4-980

Cited by 34 publications

(20 citation statements)

References 18 publications

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“…Also, glucose stimulation of rat islets induces a five-to sixfold increase in phosphoinositide hydrolysis, in sharp contrast to mouse islets in which virtually no increase was observed (5). Moreover, in rat ␤-cells, short-term exposure to high glucose induces a potentiation (priming) of the response to subsequent stimulation (6); this phenomenon is absent in mouse ␤-cells (7).…”

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confidence: 87%

Differential patterns of glucose-induced electrical activity and intracellular calcium responses in single mouse and rat pancreatic islets.

et al. 2000

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Although isolated rat islets are widely used to study in vitro insulin secretion and the underlying metabolic and ionic processes, knowledge on the properties of glucose-induced electrical activity (GIEA), a key step in glucose-response coupling, has been gathered almost exclusively from microdissected mouse islets. Using a modified intracellular recording technique, we have now compared the patterns of GIEA in collagenase-isolated rat and mouse islets. Resting membrane potentials of rat and mouse ␤-cells were approximately -50 and -60 mV, respectively. Both rat and mouse ␤-cells displayed prompt membrane depolarizations in response to glucose. However, whereas the latter exhibited a bursting pattern consisting of alternating hyperpolarized and depolarized active phases, rat ␤-cells fired action potentials from a nonoscillating membrane potential at all glucose concentrations (8.4-22.0 mmol/l). This was mirrored by changes in the intracellular Ca 2+ concentration ([Ca 2+ ] i ), which was oscillatory in mouse and nonoscillatory in rat islets. Stimulated rat ␤-cells were strongly hyperpolarized by diazoxide, an activator of ATP-dependent K + channels. Glucose evoked dosedependent depolarizations and [Ca 2+ ] i increases in both rat (EC 50 5.9-6.9 mmol/l) and mouse islets (EC 50 8.3-9.5 mmol/l), although it did not affect the burst plateau potential in the latter case. We conclude that there are important differences between ␤-cells from both species with respect to early steps in the stimulussecretion coupling cascade based on the following findings: 1) mouse ␤-cells have a larger resting K + conductance in 2 mmol/l glucose, 2) rat ␤-cells lack the compensatory mechanism responsible for generating membrane potential oscillations and holding the depolarized plateau potential in mouse ␤-cells, and 3) the electrical and [Ca 2+ ] i dose-response curves in rat ␤-cells are shifted toward lower glucose concentrations. Exploring the molecular basis of these differences may clarify several a priori assumptions on the electrophysiological properties of rat ␤-cells, which could foster the development of new working models of pancreatic ␤-cell function.

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confidence: 87%

Differential patterns of glucose-induced electrical activity and intracellular calcium responses in single mouse and rat pancreatic islets.

et al. 2000

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“…cAMP has been suggested to regulate a long-term effect of glucose on insulin secretion (Howell et al, 1973). Grill and Rundfeldt (1979) have proposed that islets have a memory for glucose exposure that results in increased responsiveness to subsequent stimulation by glucose. Presently, it remains obscure whether the sensitized effect of aminohexose is the same as that of glucose.…”

Section: Maintenance Of Neonatal Rat B Cells 571mentioning

confidence: 99%

Maintenance of pancreatic endocrine cells of the neonatal rat: VII. The effect of 3-amino-3-deoxyglucose on insulin secretion from perifused B cells.

et al. 1986

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“…These compounds induce a memory, which remains after the compound is removed, and enhances subsequent secretory responses of the ␤-cell. Once induced, TDP enhances insulin secretion in response to all secretagogues (both metabolic and nonmetabolic) in a nonspecific manner, bringing about a general strengthening of the secretory capacity of the ␤-cell (12,26,28). Only certain secretagogues can induce TDP, and a common feature among them is the ability to enhance mitochondrial metabolism and anaplerotic input, i.e., to provide intermediates into the TCA cycle (30).…”

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Dimethyl amiloride improves glucose homeostasis in mouse models of type 2 diabetes

Gunawardana

Head

Piston

2008

American Journal of Physiology-Endocrinology and Metabolism

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Dimethyl amiloride (DMA) enhances insulin secretion in the pancreatic beta-cell. DMA also enhances time-dependent potentiation (TDP) and enables TDP to occur in situations where it is normally absent. As we have demonstrated before, these effects are mediated in part through inhibition of neuronal nitric oxide synthase (nNOS), resulting in increased availability of arginine. Thus both DMA and arginine have the potential to correct the secretory defect in diabetes by enabling or enhancing TDP. In the current study we have demonstrated the ability of these agents to improve blood glucose homeostasis in three mouse models of type 2 diabetes. The pattern of TDP under different conditions indicates that inhibition of NOS is not the only mechanism through which DMA exerts its positive effects. Thus we also have explored another possible mechanism through which DMA enables/enhances TDP, via the activation of mitochondrial alpha-ketoglutarate dehydrogenase.

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Effects of Priming with D-Glucose on Insulin Secretion from Rat Pancreatic Islets: Increased Responsiveness to Other Secretagogues*

Cited by 34 publications

References 18 publications

Differential patterns of glucose-induced electrical activity and intracellular calcium responses in single mouse and rat pancreatic islets.

Differential patterns of glucose-induced electrical activity and intracellular calcium responses in single mouse and rat pancreatic islets.

Maintenance of pancreatic endocrine cells of the neonatal rat: VII. The effect of 3-amino-3-deoxyglucose on insulin secretion from perifused B cells.

Dimethyl amiloride improves glucose homeostasis in mouse models of type 2 diabetes

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