The role of old age in the effects of glucose on insulin secretion, pentosephosphate shunt activity, pyridine nucleotides and glutathione of rat pancreatic islets

Ammon, H. P. T.; Amm, U.; Eujen, R.; Hoppe, E.; Trier, G.; Verspohl, Eugen J.

doi:10.1016/0024-3205(84)90596-4

Cited by 22 publications

(13 citation statements)

References 37 publications

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“…Investigations by Elahi et al (79,Reaven and Reaven (76), Sartin et al (77), and Castro (17), have demonstrated attenuated glucose oxidation concomitant with diminished insulin secretion in islets isolated from older versus younger rats. In contrast, Ammon et al (78) reported no differences in glucose utilization nor in NADPH production in islets from old rats as compared to islets from younger animals. Burch et al (23) observed an increased glucose oxidation rate which was associated with enhanced glucokinase, phosphofructokinase, and glucose-6-phosphate dehydrogenase activity in islets of 18-month-old rats compared with 8-month-old animals.…”

Section: Glucose Oxidation Insulin Secretion and Agingmentioning

confidence: 84%

Aging and Insulin Secretion

Coordt¹,

Ruhe²,

McDonald³

1995

Experimental Biology and Medicine

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Aging in mammals has often been associated with decreased insulin secretion and a subsequent deterioration in the ability to maintain glucose homeostasis. However, recent studies have demonstrated that factors such as disease, obesity, and physical activity more closely reflect diminished insulin secretion rather than aging per se. Thus, the purpose of this article is to review recent studies of how biological aging, i.e. the process independent of disease states such as type II diabetes, may affect insulin secretion. To this end, this review will address the impact of aging on insulin secretion in terms of in vivo and in vitro assessment, as well as possible age-related alterations in the hormonal and neural regulation of insulin secretion. Finally, this review describes some evidence that alterations in the functional heterogeneity of the beta-cell population may represent a means by which the endocrine pancreas is able to maintain appropriate insulin secretion during senescence.

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Section: Glucose Oxidation Insulin Secretion and Agingmentioning

confidence: 84%

Aging and Insulin Secretion

Coordt¹,

Ruhe²,

McDonald³

1995

Experimental Biology and Medicine

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“…Notwithstanding, it has been suggested that amplification of GSIS by the gut hormone cholecystokinin involves increased pentose phosphate pathway activity [53]. Moreover, reduced pentose phosphate pathway activity reduces GSIS in islets from old animals [54], and its perturbation has been implicated in glucotoxicity [55,56]. Indeed, patients with glucose-6-phosphate dehydrogenase deficiency exhibit impaired insulin secretion [57].…”

Section: Discussionmentioning

confidence: 98%

Time-resolved metabolomics analysis of β-cells implicates the pentose phosphate pathway in the control of insulin release

Sartipy

Sharoyko

Goehring

et al. 2013

Biochemical Journal

106

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Insulin secretion is coupled with changes in β-cell metabolism. To define this process, 195 putative metabolites, mitochondrial respiration, NADP+, NADPH and insulin secretion were measured within 15 min of stimulation of clonal INS-1 832/13 β-cells with glucose. Rapid responses in the major metabolic pathways of glucose occurred, involving several previously suggested metabolic coupling factors. The complexity of metabolite changes observed disagreed with the concept of one single metabolite controlling insulin secretion. The complex alterations in metabolite levels suggest that a coupling signal should reflect large parts of the β-cell metabolic response. This was fulfilled by the NADPH/NADP+ ratio, which was elevated (8-fold; P<0.01) at 6 min after glucose stimulation. The NADPH/NADP+ ratio paralleled an increase in ribose 5-phosphate (>2.5-fold; P<0.001). Inhibition of the pentose phosphate pathway by trans-dehydroepiandrosterone (DHEA) suppressed ribose 5-phosphate levels and production of reduced glutathione, as well as insulin secretion in INS-1 832/13 β-cells and rat islets without affecting ATP production. Metabolite profiling of rat islets confirmed the glucose-induced rise in ribose 5-phosphate, which was prevented by DHEA. These findings implicate the pentose phosphate pathway, and support a role for NADPH and glutathione, in β-cell stimulus-secretion coupling.

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“…This interpretation is supported by our observations with Dia, which caused a comparable decrease in E GSH , activated chemoreceptor cells in normoxia, but not in hypoxia. In this context it is worth mentioning that Dia has variable effects on insulin release; with some secretagogues it promoted and with some others it did not affect insulin release (3). It should also be mentioned that Dia inhibited hypoxic pulmonary and prostaglandin F 2␣ vasoconstriction (59), implying an effect nonspecifically linked to hypoxic response.…”

Section: Discussionmentioning

confidence: 97%

General redox environment and carotid body chemoreceptor function

Agapito

Sanz-Alfayate²,

Gomez-Niño³

et al. 2009

American Journal of Physiology-Cell Physiology

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Carotid body (CB) chemoreceptor cells detect physiological levels of hypoxia and generate a hyperventilation, homeostatic in nature, aimed to minimize the deleterious effects of hypoxia. Intimate mechanisms involved in oxygen sensing in chemoreceptor cells remain largely unknown, but reactive oxygen species (ROS) had been proposed as mediators of this process. We have determined glutathione levels and calculated glutathione redox potential (E(GSH); indicator of the general redox environment of cells) in rat diaphragms incubated in the presence of oxidizing agents of two types: nonpermeating and permeating through cell membranes; in the latter group, unspecific oxidants and inhibitors of ROS-disposing enzymes were used. Selected concentrations of oxidizing agents were tested for their ability to modify the normoxic and hypoxic activity of chemoreceptor cells measured in vitro as their rate of release of neurotransmitters. Results evidence variable relationships between E(GSH) and the activity of chemoreceptor cells. The independence of chemoreceptor cell activity from the E(GSH) would imply that the ability of the CB to play its homeostatic role is largely preserved in any pathological or toxicological contingency causing oxidative stress. Consistent with this suggestion, it was also found that CB-mediated hypoxic hyperventilation was not altered by treatment of intact animals with agents that markedly decreased the E(GSH) in all tissues assayed.

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The role of old age in the effects of glucose on insulin secretion, pentosephosphate shunt activity, pyridine nucleotides and glutathione of rat pancreatic islets

Cited by 22 publications

References 37 publications

Aging and Insulin Secretion

Aging and Insulin Secretion

Time-resolved metabolomics analysis of β-cells implicates the pentose phosphate pathway in the control of insulin release

General redox environment and carotid body chemoreceptor function

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