scholarly journals Saturated Fatty Acids Synergize with Elevated Glucose to Cause Pancreatic β-Cell Death

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 4154-4163 ◽  
Author(s):  
Wissal El-Assaad ◽  
Jean Buteau ◽  
Marie-Line Peyot ◽  
Christopher Nolan ◽  
Raphael Roduit ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Death ◽  
Saturated Fatty Acids ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Elevated Glucose

scholarly journals Omega-3 Polyunsaturated Fatty Acids May Attenuate Streptozotocin-Induced Pancreatic β-Cell Death via Autophagy Activation in Fat1 Transgenic Mice

2015 ◽  
Vol 30 (4) ◽  
pp. 569 ◽  
Author(s):  
Won-Min Hwang ◽  
Dong-Ho Bak ◽  
Dong Ho Kim ◽  
Ju Young Hong ◽  
Seung-Yun Han ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Death ◽  
Transgenic Mice ◽  
Polyunsaturated Fatty Acids ◽  
Pancreatic Β Cell ◽  
Omega 3 ◽  
Β Cell

scholarly journals The Myokine Irisin Is Released in Response to Saturated Fatty Acids and Promotes Pancreatic β-Cell Survival and Insulin Secretion

Diabetes ◽  
2017 ◽  
Vol 66 (11) ◽  
pp. 2849-2856 ◽  
Author(s):  
Annalisa Natalicchio ◽  
Nicola Marrano ◽  
Giuseppina Biondi ◽  
Rosaria Spagnuolo ◽  
Rossella Labarbuta ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Cell Survival ◽  
Saturated Fatty Acids ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e22485 ◽  
Author(s):  
J. Jason Collier ◽  
Susan J. Burke ◽  
Mary E. Eisenhauer ◽  
Danhong Lu ◽  
Renee C. Sapp ◽  
...  
Keyword(s):  
Cell Death ◽  
Inflammatory Cytokines ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Pro Inflammatory Cytokines

Effects of pharmacological inhibition of NADPH oxidase or iNOS on pro-inflammatory cytokine, palmitic acid or H2O2-induced mouse islet or clonal pancreatic β-cell dysfunction

2010 ◽  
Vol 30 (6) ◽  
pp. 445-453 ◽  
Author(s):  
Marta Michalska ◽  
Gabriele Wolf ◽  
Reinhard Walther ◽  
Philip Newsholme
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Nadph Oxidase ◽  
Inflammatory Cytokine ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Mouse Islets ◽  
Pro Inflammatory Cytokines

Various pancreatic β-cell stressors including cytokines and saturated fatty acids are known to induce oxidative stress, which results in metabolic disturbances and a reduction in insulin secretion. However, the key mechanisms underlying dysfunction are unknown. We investigated the effects of prolonged exposure (24 h) to pro-inflammatory cytokines, H2O2 or PA (palmitic acid) on β-cell insulin secretion, ATP, the NADPH oxidase (nicotinamide adenine dinucleotide phosphate oxidase) component p47phox and iNOS (inducible nitric oxide synthase) levels using primary mouse islets or clonal rat BRIN-BD11 β-cells. Addition of a pro-inflammatory cytokine mixture [IL-1β (interleukin-1β), TNF-α (tumour necrosis factor-α) and IFN-γ (interferon-γ)] or H2O2 (at sub-lethal concentrations) inhibited chronic (24 h) levels of insulin release by at least 50% (from islets and BRIN-BD11 cells), while addition of the saturated fatty acid palmitate inhibited acute (20 min) stimulated levels of insulin release from mouse islets. H2O2 decreased ATP levels in the cell line, but elevated p47phox and iNOS levels as did cytokine addition. Similar effects were observed in mouse islets with respect to elevation of p47phox and iNOS levels. Addition of antioxidants SOD (superoxide dismutase), Cat (catalase) and NAC (N-acetylcysteine) attenuated H2O2 or the saturated fatty acid palmitate-dependent effects, but not cytokine-induced dysfunction. However, specific chemical inhibitors of NADPH oxidase and/or iNOS appear to significantly attenuate the effects of cytokines, H2O2 or fatty acids in islets. While pro-inflammatory cytokines are known to increase p47phox and iNOS levels in β-cells, we now report that H2O2 can increase levels of the latter two proteins, suggesting a key role for positive-feedback redox sensitive regulation of β-cell dysfunction.

scholarly journals Distinctive postprandial modulation of β cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

2008 ◽  
Vol 88 (3) ◽  
pp. 638-644 ◽  
Author(s):  
Sergio López ◽  
Beatriz Bermúdez ◽  
Yolanda M Pacheco ◽  
José Villar ◽  
Rocío Abia ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Saturated Fatty Acids ◽  
Dietary Fats ◽  
Β Cell ◽  
Β Cell Function

Estrogen reduces endoplasmic reticulum stress to protect against glucotoxicity induced-pancreatic β-cell death

2014 ◽  
Vol 139 ◽  
pp. 25-32 ◽  
Author(s):  
Suwattanee Kooptiwut ◽  
Pitchnischa Mahawong ◽  
Wanthanee Hanchang ◽  
Namoiy Semprasert ◽  
Suchada Kaewin ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Antagonism Between Saturated and Unsaturated Fatty Acids in ROS Mediated Lipotoxicity in Rat Insulin-Producing Cells

2015 ◽  
Vol 36 (3) ◽  
pp. 852-865 ◽  
Author(s):  
Wiebke Gehrmann ◽  
Wiebke Würdemann ◽  
Thomas Plötz ◽  
Anne Jörns ◽  
Sigurd Lenzen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Palmitic Acid ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
H2o2 Production ◽  
Β Cell ◽  
Specific Expression ◽  
Insulin Producing Cells ◽  
H2o2 Formation

Background/Aims: Elevated levels of non-esterified fatty acids (NEFAs) are under suspicion to mediate β-cell dysfunction and β-cell loss in type 2 diabetes, a phenomenon known as lipotoxicity. Whereas saturated fatty acids show a strong cytotoxic effect upon insulin-producing cells, unsaturated fatty acids are not toxic and can even prevent toxicity. Experimental evidence suggests that oxidative stress mediates lipotoxicity and there is evidence that the subcellular site of ROS formation is the peroxisome. However, the interaction between unsaturated and saturated NEFAs in this process is unclear. Methods: Toxicity of rat insulin-producing cells after NEFA incubation was measured by MTT and caspase assays. NEFA induced H2O2 formation was quantified by organelle specific expression of the H2O2 specific fluorescence sensor protein HyPer. Results: The saturated NEFA palmitic acid had a significant toxic effect on the viability of rat insulin-producing cells. Unsaturated NEFAs with carbon chain lengths >14 showed, irrespective of the number of double bonds, a pronounced protection against palmitic acid induced toxicity. Palmitic acid induced H2O2 formation in the peroxisomes of insulin-producing cells. Oleic acid incubation led to lipid droplet formation, but in contrast to palmitic acid induced neither an ER stress response nor peroxisomal H2O2 generation. Furthermore, oleic acid prevented palmitic acid induced H2O2 production in the peroxisomes. Conclusion: Thus unsaturated NEFAs prevent deleterious hydrogen peroxide generation during peroxisomal β-oxidation of long-chain saturated NEFAs in rat insulin-producing cells.

scholarly journals Autophagy couteracts weight gain, lipotoxicity and pancreatic β-cell death upon hypercaloric pro-diabetic regimens

2017 ◽  
Vol 8 (8) ◽  
pp. e2970-e2970 ◽  
Author(s):  
Álvaro F Fernández ◽  
Clea Bárcena ◽  
Gemma G Martínez-García ◽  
Isaac Tamargo-Gómez ◽  
María F Suárez ◽  
...  
Keyword(s):  
Cell Death ◽  
Weight Gain ◽  
Pancreatic Β Cell ◽  
Β Cell

Cadmium exposure induces pancreatic β-cell death via a Ca2+-triggered JNK/CHOP-related apoptotic signaling pathway

Toxicology ◽  
2019 ◽  
Vol 425 ◽  
pp. 152252 ◽  
Author(s):  
Cheng-Chin Huang ◽  
Chun-Ying Kuo ◽  
Ching-Yao Yang ◽  
Jui-Ming Liu ◽  
Ren-Jun Hsu ◽  
...  
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Cadmium Exposure ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Apoptotic Signaling
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