Effect of Amino Acids and Proteins on Insulin Secretion in Man

Fajans, Stefan S.; Floyd, John C.; Knopf, Ralph F.; Conn, Jerome W.

doi:10.1016/b978-0-08-013395-9.50021-6

Cited by 43 publications

(61 citation statements)

References 12 publications

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“…27 Similarly, children with HI caused by partial mutations of the K ATP channel show enhanced insulin responses to leucine stimulation. 24 These findings suggest that partial ␤-cell membrane depolarization, by either genetic defects or drug administration, lowers the threshold for leucine-stimulated insulin secretion by increasing sensitivity to changes in ATP/ADP.…”

Section: Discussionmentioning

confidence: 98%

Protein-sensitive hypoglycemia without leucine sensitivity in hyperinsulinism caused by KATP channel mutations

Fourtner

Stanley

Kelly

2006

The Journal of Pediatrics

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Section: Discussionmentioning

confidence: 98%

Protein-sensitive hypoglycemia without leucine sensitivity in hyperinsulinism caused by KATP channel mutations

Fourtner

Stanley

Kelly

2006

The Journal of Pediatrics

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“…Using 13 C-labelled glutamine and NMR spectroscopy, we [34] have shown that the major products of l-[1,2 13 C]glutamine metabolism are l-[1,2 13 C]glutamate and l-aspartate labelled at positions C 1 and C 4 in BRIN-BD11 cells. l-Aspartate is formed after entry of lglutamate into the TCA cycle.…”

Section: Mechanisms Of Amino-acid-dependent Stimulation Of Insulin Sementioning

confidence: 98%

“…Thus a relatively small number of amino acids promote or synergistically enhance insulin release from pancreatic β-cells [13,14]. The mechanisms by which amino acids enhance insulin secretion are varied.…”

Section: Figure 1 Model For the Regulation Of Insulin Secretion In Thmentioning

confidence: 99%

New insights into amino acid metabolism, β-cell function and diabetes

Newsholme

Brennan

Rubı́³

et al. 2005

Clinical Science

234

184

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Specific amino acids are now known to acutely and chronically regulate insulin secretion from pancreatic beta-cells in vivo and in vitro. Understanding the molecular mechanisms by which amino acids regulate insulin secretion may identify novel targets for future diabetes therapies. Mitochondrial metabolism is crucial for the coupling of amino acid and glucose recognition to the exocytosis of the insulin granules. This is illustrated by in vitro and in vivo observations discussed in the present review. Mitochondria generate ATP, which is the main coupling factor in insulin secretion; however, the subsequent Ca2+ signal in the cytosol is necessary, but not sufficient, for full development of sustained insulin secretion. Hence mitochondria generate ATP and other coupling factors serving as fuel sensors for the control of the exocytotic process. Numerous studies have sought to identify the factors that mediate the amplifying pathway over the Ca2+ signal in nutrient-stimulated insulin secretion. Predominantly, these factors are nucleotides (GTP, ATP, cAMP and NADPH), although metabolites have also been proposed, such as long-chain acyl-CoA derivatives and the key amino acid glutamate. This scenario highlights further the importance of the key enzymes or transporters, glutamate dehydrogenase, the aspartate and alanine aminotransferases and the malate/aspartate shuttle, in the control of insulin secretion. Therefore amino acids may play a direct or indirect (via generation of putative messengers of mitochondrial origin) role in insulin secretion.

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“…Although amino acids, and in particular arginine, can serve as insulin secretagogues [23] and may contribute to fetal hyperinsulinaemia in diabesity, glucose is the most important stimulator of insulin secretion. Thus, this has sparked research interest trying to understand the regulation of maternal-tofetal glucose transport across the placenta.…”

Section: The Fetal Phenotype In Diabesitymentioning

confidence: 99%