Autocrine/Paracrine Function of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) for Glucose Homeostasis in Pancreatic β-Cells and Adipocytes

Park, Kwang‐Hyun; Kim, Byung-Ju; Shawl, Asif Iqbal; Han, Myung‐Kwan; Lee, Hon Cheung; Kim, Uh-Hyun

doi:10.1074/jbc.m113.489278

Cited by 28 publications

(26 citation statements)

References 37 publications

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“…In line with our previous report that NAADP has paracrine functions in glucose homeostasis (37), it would be interesting to know whether exercise brings additional benefits for glucose homeostasis, specifically if the increased NAADP levels in skeletal muscle during exercise could be released into the blood stream through cell damage or another unidentified mechanism, NAADP would act on pancreas b-cells and adipocytes for insulin secretion and glucose uptake, respectively.…”

Section: Discussionmentioning

confidence: 90%

Exercise Ameliorates Insulin Resistance via Ca2+ Signals Distinct From Those of Insulin for GLUT4 Translocation in Skeletal Muscles

Park

Kim

et al. 2014

Diabetes

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Muscle contraction and insulin induce glucose uptake in skeletal muscle through GLUT4 membrane translocation. Beneficial effects of exercise on glucose homeostasis in insulin-resistant individuals are known to be due to their distinct mechanism between contraction and insulin action on glucose uptake in skeletal muscle. However, the underlying mechanisms are not clear. Here we show that in skeletal muscle, distinct Ca 2+ second messengers regulate GLUT4 translocation by contraction and insulin treatment; D-myo-inositol 1,4,5-trisphosphate/nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose/NAADP are main players for insulin-and contraction-induced glucose uptake, respectively. Different patterns of phosphorylation of AMPK and Ca 2+ /calmodulindependent protein kinase II were shown in electrical stimuli (ES)-and insulin-induced glucose uptake pathways. ES-induced Ca 2+ signals and glucose uptake are dependent on glycolysis, which influences formation of NAD(P)-derived signaling messengers, whereas insulininduced signals are not. High-fat diet (HFD) induced a defect in only insulin-mediated, but not ES-mediated, Ca 2+ signaling for glucose uptake, which is related to a specifically lower NAADP formation. Exercise decreases blood glucose levels in HFD-induced insulin resistance mice via NAADP formation. Thus we conclude that different usage of Ca 2+ signaling in contraction/insulin-stimulated glucose uptake in skeletal muscle may account for the mechanism by which exercise ameliorates glucose homeostasis in individuals with type 2 diabetes.Both insulin and contraction induce the translocation of GLUT4 from the interior of the muscle cell to the cell membrane, leading to an increase in glucose uptake into the muscle cell (1,2). However, evidence indicates that contraction-induced GLUT4 translocation uses a mechanism distinct from that of insulin (3,4). This is the basis behind the beneficial effects of exercise in cases where insulin resistance is present, such as type 2 diabetes (5,6). However, the exact mechanisms by which insulin and contraction induce glucose transport are not clear. Ca 2+ plays a versatile role in intracellular signaling (7). Mammalian cells have specific Ca 2+ signals for particular cellular processes. Ca 2+ second messengers control intracellular Ca 2+ levels by mobilizing Ca 2+ from intracellular stores, including the sarcoplasmic reticulum, lysosomes, and mitochondria (8). D-myo-inositol 1,4,5-trisphosphate (IP 3 ), cyclic ADP-ribose (cADPR), and nicotinic acid adenine dinucleotide phosphate (NAADP) are well-characterized Ca 2+ second messengers. IP 3 is produced by phospholipase C, and the latter two by ADP-ribosyl cyclases, including CD38 (9-11). Ca 2+ signals in skeletal muscle mediate a variety of physiological processes, including muscle contraction and cell metabolism

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Section: Discussionmentioning

confidence: 90%

Exercise Ameliorates Insulin Resistance via Ca2+ Signals Distinct From Those of Insulin for GLUT4 Translocation in Skeletal Muscles

Park

Kim

et al. 2014

Diabetes

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“…Inactivation or inhibition of NAADP receptors blunted the glucose-induced [Ca 2+ ] c rise [123] [221,224]. NAADP has recently been suggested to act as an autocrine or paracrine signal for ␤-cell since its extracellular application at submicromolar concentrations increased [Ca 2+ ] c possibly as a result of its uptake by the cell [225]. A release of Ca 2+ from endo/lysosomes independent of NAADP and involving RyR has also been suggested in ␤-cells [132].…”

Section: Acidic Ca 2+ Storesmentioning

confidence: 99%

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

et al. 2014

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“…2 (23) and in a rat basophilic cell line (24). Recent reports further showed that exogenous NAADP was transported into human lymphokine-activated killer cells and induced Ca 2ϩ release from lysosomal-like acidic stores in those cells (25) and in mouse pancreatic ␤ cells and adipocytes (26). These observations prompted us to test this approach to investigate the NAADP-mediated Ca 2ϩ release mechanism in a more specific manner through direct activation of Ca 2ϩ release in naive T cells by NAADP.…”

Section: Naadpmentioning

confidence: 99%

“…We examined uptake of external NAADP into the cells by a [ 32 P]NAADP transport experiment similar to that used to demonstrate uptake by pancreatic ␤ cells (26) and LAK cells (25). CD4 T cells showed a concentration and time-dependent increase in [ 32 P]NAADP (Fig.…”

Section: Naadpmentioning

confidence: 99%

“…3H, the Ca 2ϩ signal was reduced to half after blocking these channels with either inhibitor, which indicates a positive role of these channels in importing NAADP into the cell, but also suggests the existence of another transporter. In fact, it has been suggested that NAADP has specific nucleoside transporters (24,26). To test the role of nucleoside transporters, we used a saturating concentration of dipyridamole, a nucleoside transport inhibitor, to ensure blockage of these transporters.…”

Section: Naadpmentioning

confidence: 99%

See 1 more Smart Citation

Nicotinic Acid Adenine Dinucleotide Phosphate Plays a Critical Role in Naive and Effector Murine T Cells but Not Natural Regulatory T Cells

Ali¹,

Camick²,

Wiles³

et al. 2016

Journal of Biological Chemistry

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Autocrine/Paracrine Function of Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) for Glucose Homeostasis in Pancreatic β-Cells and Adipocytes

Cited by 28 publications

References 37 publications

Exercise Ameliorates Insulin Resistance via Ca2+ Signals Distinct From Those of Insulin for GLUT4 Translocation in Skeletal Muscles

Exercise Ameliorates Insulin Resistance via Ca2+ Signals Distinct From Those of Insulin for GLUT4 Translocation in Skeletal Muscles

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Nicotinic Acid Adenine Dinucleotide Phosphate Plays a Critical Role in Naive and Effector Murine T Cells but Not Natural Regulatory T Cells

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