Heat Shock Restores Insulin Secretion after Injury by Nitric Oxide by Maintaining Glucokinase Activity in Rat Islets

Takeda, Tomomi; Tsuura, Yoshiyuki; Fujita, Jun; Fujimoto, Shimpei; Mukai, Eri; Kajikawa, Mariko; Hamamoto, Yoshiyuki; Kume, Makoto; Yamamoto, Yūzō; Yamaoka, Yoshio; Yamada, Yoshio; Seino, Yutaka

doi:10.1006/bbrc.2001.4933

Cited by 12 publications

(5 citation statements)

References 38 publications

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“…Our functional respiratory data reveal that IL-1β plus IFN-γ impair GSIS by restricting mitochondrial capacity for oxidising pyruvate ( Fig 2 ), which is consistent with a well-established aconites inhibition by cytokine-induced NO [ 25 , 26 ]. Reported glucokinase inhibition [ 20 – 24 ] unlikely accounts for the inflammatory GSIS phenotype we report here ( Fig 1A ) as glucose- and pyruvate-stimulated electron transfer capacity are equally sensitive to IL-1β plus IFN-γ. Restricted pyruvate oxidation capacity dampens glucose sensitivity ( Fig 2B ) and coupling efficiency of oxidative phosphorylation ( Fig 2C ), and thus likely prevents an increase in the ATP/ADP ratio that initiates the electrophysiological events that are necessary for Ca 2+ influx and eventual exocytosis of insulin-containing granules.…”

Section: Discussionmentioning

confidence: 88%

“…Cytokine-induced β-cell failure is likely mediated by nitric oxide (NO) that results from activation of inducible nitric oxide synthase [ 16 ], but NO-independent inflammatory mechanisms have also been suggested [ 17 – 19 ]. Cytokine-provoked NO may inhibit glycolysis [ 20 – 24 ] and/or the mitochondrial TCA cycle [ 25 , 26 ], but functional bioenergetic consequences of such inhibition have not been demonstrated to date. It is worth notice in this respect that NO may in fact benefit the bioenergetics of inflamed cells as it stimulates mitochondrial biogenesis under certain circumstances [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

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Pro-inflammatory cytokines attenuate glucose-stimulated insulin secretion from INS-1E insulinoma cells by restricting mitochondrial pyruvate oxidation capacity – Novel mechanistic insight from real-time analysis of oxidative phosphorylation

2018

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Pro-inflammatory cytokines cause pancreatic beta cell failure during the development of type 2 diabetes. This beta cell failure associates with mitochondrial dysfunction, but the precise effects of cytokines on mitochondrial respiration remain unclear. To test the hypothesis that pro-inflammatory cytokines impair glucose-stimulated insulin secretion (GSIS) by inhibiting oxidative ATP synthesis, we probed insulin release and real-time mitochondrial respiration in rat INS-1E insulinoma cells that were exposed to a combination of 2 ng/mL interleukin-1-beta and 50 ng/mL interferon-gamma. We show that 24-h exposure to these cytokines dampens both glucose- and pyruvate-stimulated insulin secretion (P < 0.0001 and P < 0.05, respectively), but does not affect KCl-induced insulin release. Mirroring secretory defects, glucose- and pyruvate-stimulated mitochondrial respiration are lowered after cytokine exposure (P < 0.01). Further analysis confirms that cytokine-induced mitochondrial respiratory defects occur irrespective of whether fuel oxidation is coupled to, or uncoupled from, ATP synthesis. These observations demonstrate that pro-inflammatory cytokines attenuate GSIS by restricting mitochondrial pyruvate oxidation capacity. Interleukin-1-beta and interferon-gamma also increase mitochondrial superoxide levels (P < 0.05), which may reinforce the inhibition of pyruvate oxidation, and cause a modest (20%) but significant (P < 0.01) loss of INS-1E cells. Cytokine-induced INS-1E cell failure is insensitive to palmitoleate and linoleate, which is at odds with the cytoprotection offered by unsaturated fatty acids against harm caused by nutrient excess. Our data disclose a mitochondrial mechanism for cytokine-impaired GSIS in INS-1E cells, and suggest that inflammatory and nutrient-related beta cell failure emerge, at least partly, through distinct paths.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Pro-inflammatory cytokines attenuate glucose-stimulated insulin secretion from INS-1E insulinoma cells by restricting mitochondrial pyruvate oxidation capacity – Novel mechanistic insight from real-time analysis of oxidative phosphorylation

2018

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“…This could avoid cow produce more heat in hot environments. On the other hand, Lactonin increased insulin concentration, which helped cow to maintain a more normal metabolism in hot summer and induced the expression of heat-shock protein gene hsp70 (Takeda et al, 2001). Taken together, Lactonin facilitates dairy cow adapted to hot environments and improves cow performance.…”

Section: Discussionmentioning

confidence: 92%

Effects of cysteamine compound on milk production and hormonal responses of lactating cow during heat stress

Shen¹,

Zhang²

2004

J. Anim. Feed Sci.

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“…Some perspectives suggest that hyperglycemia in diabetic patients may trigger increased iHSP70 expression, potentially leading to cellular damage ( 43 ). On the contrary, others posit that the decrease in iHSP70 reduces the protective function of pancreatic β-cells, further leading to their impairment and the eventual development of Type 2 diabetes ( 44 ). Given the asynchronous patterns of eHSP70 and iHSP70, Krause M and colleagues presented an intriguing concept concerning the chaperone balance hypothesis.…”

Section: Potential Link Between Cuproptosis and Diabetesmentioning

confidence: 99%

Cuproptosis: potential new direction in diabetes research and treatment

Qu,

Wang,

Wang

2024

Front. Endocrinol.

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Cuproptosis, a recently discovered form of cell death, stems from an overabundance of copper ions infiltrating mitochondria. These ions directly engage lipoylated proteins, prompting their oligomerization and subsequent loss of iron-sulfur clusters. This sequence induces proteotoxic stress, ultimately culminating in cell death. Type 2 diabetes, a chronic metabolic disorder resulting from a complex interplay of genetic and environmental factors, has not yet been fully understood in terms of its etiology and pathogenesis. Intricately, it is linked to various modalities of cell death, including mitochondrial autophagy, apoptosis, pyroptosis, and ferroptosis. Studies have discovered impaired copper metabolism in individuals with Type 2 diabetes, hinting at a unique role for copper homeostasis in the progression of the disease. To this end, the present research aims to delineate the potential correlation between cuproptosis and Type 2 diabetes by exhaustively reviewing the existing literature. By synthesizing relevant research on cuproptosis, the paper intends to lay the groundwork for a thorough exploration of the pathogenesis of Type 2 diabetes and the development of targeted therapeutic interventions. The ultimate objective is to facilitate a deeper understanding of Type 2 diabetes and to identify novel therapeutic strategies associated with cuproptosis.

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Heat Shock Restores Insulin Secretion after Injury by Nitric Oxide by Maintaining Glucokinase Activity in Rat Islets

Cited by 12 publications

References 38 publications

Pro-inflammatory cytokines attenuate glucose-stimulated insulin secretion from INS-1E insulinoma cells by restricting mitochondrial pyruvate oxidation capacity – Novel mechanistic insight from real-time analysis of oxidative phosphorylation

Pro-inflammatory cytokines attenuate glucose-stimulated insulin secretion from INS-1E insulinoma cells by restricting mitochondrial pyruvate oxidation capacity – Novel mechanistic insight from real-time analysis of oxidative phosphorylation

Effects of cysteamine compound on milk production and hormonal responses of lactating cow during heat stress

Cuproptosis: potential new direction in diabetes research and treatment

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