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N H McClenaghan, C R Barnett, F P M O'Harte and P R Flatt

Abstract

The effects of different classes of amino acids known to be transported and utilized by pancreatic B-cells were examined using the novel glucose-responsive pancreatic B-cell line, BRIN-BD11. Amino acids tested included α-aminoisobutyric acid, l-alanine, l-arginine, l-glutamine, glycine, l-leucine, l-lysine, l-proline and l-serine. At non-stimulatory (1·1 mmol/l) glucose, acute incubations with either 1 or 10 mmol/l amino acid evoked 1·3- to 4·7-fold increases of insulin release. Raising glucose to 16·7 mmol/l enhanced the effects of all amino acids except l-glutamine, and increased insulin output at 10 mmol/l compared with 1 mmol/l amino acid. Glyceraldehyde (10 mmol/l) also served to promote 10 mmol/l amino acid-induced insulin secretion with the exceptions of l-arginine, glycine, l-lysine and l-proline. At 16·7 mmol/l glucose, diazoxide (300 μmol/l) significantly decreased the secretory response to all amino acids except l-glutamine. Likewise, verapamil (20 μmol/l) or depletion of extracellular Ca2+ reduced insulin output indicating the importance of Ca2+ influx in the actions of amino acids. These data indicate that BRIN-BD11 cells transport and utilize amino acids, acting in association with glycolysis, K+-ATP channels and/or voltage-dependent Ca2+ channels to promote Ca2+ influx and insulin secretion. The response of BRIN-BD11 cells to glucose and amino acids indicates that this is a useful cell line for future research on the mechanisms of nutrient regulation of insulin secretion.

Journal of Endocrinology (1996) 151, 349–357

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J. Hinson and M. K. Birmingham

ABSTRACT

The effects of the dibutyryl derivatives of cyclic GMP and cyclic AMP on lactic acid and steroid production were compared in intact mouse adrenal glands at concentrations of 0·5–1 mmol/l and in mouse adrenal cell suspensions at concentrations of 0·01–1 mmol/l. The dibutyryl derivative of cyclic GMP had little or no effect on lactic acid production in either tissue preparation. It caused a slight stimulation of corticosteroid output in intact glands at a concentration of 1 mmol/l, amounting to one-tenth of the response observed with 1 mm-dibutyryl cyclic AMP. Dose-dependent increases in lactic acid and steroid production were obtained with dibutyryl cyclic AMP in cell suspensions. AMP and GMP increased lactic acid but not steroid production.

All the substrates tested (glucose, glucose-6-phosphate, fructose, fructose-6-phosphate, fructose-1,6-diphosphate, 10 mmol/l; pyruvate and glycerol, 20 mmol/l) stimulated basal glycolysis in intact glands and cell suspensions and none affected basal steroid production significantly. By far the greatest increase in lactic acid production was noted with fructose-1,6-diphosphate. However, only glucose and, in unsectioned glands, pyruvate exerted a potentiating effect on the glycolytic response to ACTH. Glucose potentiated the steroidogenic response to ACTH also, but only in intact glands.

The relative ineffectiveness of dibutyryl cyclic GMP is in accord with the species-dependent differing responses to the free form of the cyclic nucleotides noted in mouse and rat adrenal glands. The substrate requirements are in keeping with a rate-limiting role of phosphofructokinase and an action of ACTH at some site between the entry of glucose into the cell and the formation of fructose-1,6-diphosphate.

J. Endocr. (1985) 104, 105–111

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Sheree D Martin and Sean L McGee

reprogramming is necessary to allow cancer cells to overcome growth inhibition checkpoints and apoptotic signaling as well as fueling invasion and metastasis ( DeBerardinis & Chandel 2016 ). Increased aerobic glycolysis irrespective of oxygen availability

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Che-Pei Kung and Maureen E Murphy

insulin and overactive glycolysis. Glucotoxicity triggers DNA damage and p53 activation, which ultimately results in beta-cell death and late-onset diabetes ( Tornovsky-Babeay et al . 2014 ). Two other processes regulated by p53, endoplasmic reticulum (ER

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T C Alba-Loureiro, S M Hirabara, J R Mendonça, R Curi and T C Pithon-Curi

. 1986 ). Decreased rates of glycolysis and glycogen synthesis were observed in leukocytes of diabetic patients. These changes are abolished by in vivo insulin administration ( Esmann 1983 ). Walrand et al. (2004) postulated that insulin may

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Lucy M Hinder, Anuradha Vivekanandan-Giri, Lisa L McLean, Subramaniam Pennathur and Eva L Feldman

 min), allowing comparative results within this study. Targeted metabolomic analysis by LC/MS/MS Frozen tissue samples were extracted with 150 μl of chilled 8:1:1 methanol:chloroform:water containing 13 C-labeled glycolysis and TCA cycle standards

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Makiko Shimodahira, Shimpei Fujimoto, Eri Mukai, Yasuhiko Nakamura, Yuichi Nishi, Mayumi Sasaki, Yuichi Sato, Hiroki Sato, Masaya Hosokawa, Kazuaki Nagashima, Yutaka Seino and Nobuya Inagaki

metabolic fuel-induced insulin release independent of glycolysis, KIC-induced insulin release from rapamycin-treated islets was examined. Chronic exposure to 30 nM rapamycin decreased high KIC-induced insulin release (1.93±0.10, rapamycin versus 3.09±0.18 ng

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Isabelle Leclerc, Guy A Rutter, Gargi Meur and Nafeesa Noordeen

-term storage ( Uyeda & Repa 2006 ). Mice deleted for both alleles of Mlxipl display diminished rates of hepatic glycolysis and lipogenesis resulting in high liver glycogen content, low plasma free fatty acid and reduced adipose tissue mass ( Iizuka et al

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Mattias Gäreskog and Parri Wentzel

(ROS), which yields mitochondrial swelling and enhanced lipid peroxidation in the embryos. This is because excess pyruvate from glycolysis moves across the mitochondrial membrane, overloading the electron transport chain ( Yang et al. 1998

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Xiwen Xiong, Cuicui Zhang, Yang Zhang, Rui Fan, Xinlai Qian and X Charlie Dong

years, SIRT6 has been implicated in a variety of metabolic processes including glycolysis ( Zhong et al. 2010 ), gluconeogenesis ( Dominy et al. 2012 , Xiong et al. 2013 ), hepatic lipid ( Kim et al. 2010 ) and cholesterol metabolism ( Elhanati