Arachidonic acid and lipoxin A4 attenuate alloxan‐induced cytotoxicity to <scp>RIN5F</scp> cells <i>in vitro</i> and type 1 diabetes mellitus <i>in vivo</i>

Gundala, Naveen K.V.; Naidu, V.G.M.; Das, Undurti N.

doi:10.1002/biof.1336

Cited by 73 publications

(58 citation statements)

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“…In a series of previous studies, we showed that oral feeding of oils rich in ω-3 EPA and DHA and ω-6 GLA and AA or pure FFAs (GLA, AA, EPA, and DHA) prevent apoptosis of insulin-secreting rat insulinoma (RIN5F) cells in vitro and alloxan-induced type 1 DM and STZ-induced type 1 and type 2 DM in experimental animals ( 15 – 18 , 137 , 420 ). This beneficial action of PUFAs against chemical-induced type 1 and type 2 DM is not abrogated by COX and LOX inhibitors, suggesting that fatty acids themselves are active and/or their anti-inflammatory LXs, resolvins, protectins, and maresins may have antidiabetic actions [see Figures 6 – 8 and Ref.…”

Section: Conclusion: Pufas and Their Metabolites In Dmmentioning

confidence: 99%

“… Effect of pre-treatment with resolvin D2 and protectin and lipoxin A4 (LXA4) on streptozotocin (STZ)-induced cytotoxicity to RIN5F cells in vitro [these data are taken from Ref. ( 137 )]. (A,B) RIN5F cells were pretreated with 1, 5, 10, and 50 ng/ml of resolvin D2 and protectin, respectively to study its modulatory action on STZ (21 mM)-induced cytotoxic action.…”

Section: Pufas Lxa4 Resolvins Protectins and Type 1 Dmmentioning

confidence: 99%

“… Effect of lipoxin A4 (LXA4) on streptozotocin (STZ)-induced type 1 diabetes mellitus (type 1 DM) (A–C) and resolvin D1 on STZ-induced type 1 DM (D) [these data are taken from Ref. ( 137 ) and unpublished data]. These studies were approved by Institutional Animal Ethics committee.…”

Section: Pufas Lxa4 Resolvins Protectins and Type 1 Dmmentioning

confidence: 99%

“…This beneficial action of PUFAs against chemical-induced type 1 and type 2 DM is not abrogated by COX and LOX inhibitors, suggesting that fatty acids themselves are active and/or their anti-inflammatory LXs, resolvins, protectins, and maresins may have antidiabetic actions [see Figures 6 – 8 and Ref. ( 15 – 18 , 137 , 420 )], while pro-inflammatory PGs, LTs, and TXs are ineffective ( 131 , 132 ). Our recent studies showed that fish oil (a rich source of EPA and DHA) altered the growth of Helicobacter, Clostridiales, Sphingomonadales, Firmicutes, Pseudomonas species, and several other bacteria ( 421 ).…”

Section: Conclusion: Pufas and Their Metabolites In Dmmentioning

confidence: 99%

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Is There a Role for Bioactive Lipids in the Pathobiology of Diabetes Mellitus?

Das¹

2017

Front. Endocrinol.

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Inflammation, decreased levels of circulating endothelial nitric oxide (eNO) and brain-derived neurotrophic factor (BDNF), altered activity of hypothalamic neurotransmitters (including serotonin and vagal tone) and gut hormones, increased concentrations of free radicals, and imbalance in the levels of bioactive lipids and their pro- and anti-inflammatory metabolites have been suggested to play a role in diabetes mellitus (DM). Type 1 diabetes mellitus (type 1 DM) is due to autoimmune destruction of pancreatic β cells because of enhanced production of IL-6 and tumor necrosis factor-α (TNF-α) and other pro-inflammatory cytokines released by immunocytes infiltrating the pancreas in response to unknown exogenous and endogenous toxin(s). On the other hand, type 2 DM is due to increased peripheral insulin resistance secondary to enhanced production of IL-6 and TNF-α in response to high-fat and/or calorie-rich diet (rich in saturated and trans fats). Type 2 DM is also associated with significant alterations in the production and action of hypothalamic neurotransmitters, eNO, BDNF, free radicals, gut hormones, and vagus nerve activity. Thus, type 1 DM is because of excess production of pro-inflammatory cytokines close to β cells, whereas type 2 DM is due to excess of pro-inflammatory cytokines in the systemic circulation. Hence, methods designed to suppress excess production of pro-inflammatory cytokines may form a new approach to prevent both type 1 and type 2 DM. Roux-en-Y gastric bypass and similar surgeries ameliorate type 2 DM, partly by restoring to normal: gut hormones, hypothalamic neurotransmitters, eNO, vagal activity, gut microbiota, bioactive lipids, BDNF production in the gut and hypothalamus, concentrations of cytokines and free radicals that results in resetting glucose-stimulated insulin production by pancreatic β cells. Our recent studies suggested that bioactive lipids, such as arachidonic acid, eicosapentaneoic acid, and docosahexaenoic acid (which are unsaturated fatty acids) and their anti-inflammatory metabolites: lipoxin A4, resolvins, protectins, and maresins, may have antidiabetic actions. These bioactive lipids have anti-inflammatory actions, enhance eNO, BDNF production, restore hypothalamic dysfunction, enhance vagal tone, modulate production and action of ghrelin, leptin and adiponectin, and influence gut microbiota that may explain their antidiabetic action. These pieces of evidence suggest that methods designed to selectively deliver bioactive lipids to pancreatic β cells, gut, liver, and muscle may prevent type 1 and type 2 DM.

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Section: Conclusion: Pufas and Their Metabolites In Dmmentioning

confidence: 99%

Section: Pufas Lxa4 Resolvins Protectins and Type 1 Dmmentioning

confidence: 99%

Section: Pufas Lxa4 Resolvins Protectins and Type 1 Dmmentioning

confidence: 99%

Section: Conclusion: Pufas and Their Metabolites In Dmmentioning

confidence: 99%

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Is There a Role for Bioactive Lipids in the Pathobiology of Diabetes Mellitus?

Das¹

2017

Front. Endocrinol.

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“…Знижений вміст ліпоксину А4 у сироватці крові корелює з підвищеним ризиком розвитку метаболічного синдрому [81]. Показано, що введення АК або ліпоксину зменшує прояви цитотоксичності алоксану in vitro та розвиток алоксанової моделі ЦД у щурів in vivo [82]. Тож деякі автори розглядають ліпоксин А4 як перспективний засіб фармакологічної корекції проявів цього захворювання [83,84].…”

Section: метаболіти арахідонової кислотиunclassified

Diabetes Mellitus and Pulmonary Circulation (Part 2)

Dobrelia¹,

Khromov²

2019

Fiziol Zh

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За умов цукрового діабету (ЦД) у судинах малого кола кровообігу спостерігається ендотеліальна дисфункція з порушенням NO-залежної вазорелаксації й збільшенням концентрації ендотеліну в крові, що корелює з гіперглікемією, вмістом глікозильованого гемоглобіну, та окисним стресом. Описане значне підвищення експрессії рецепторів до ендотеліну типу А і дещо менше до рецепторів типу В у судинах легень. За умов ЦД вміст арахідонової кислоти та її метаболітів, а також реакції судин на них суттєво змінені: посилені утворення та екскреція констрикторних чинників, а вплив вазорелаксантів зменшений. Дані щодо змін вмісту та впливу на реакції судин гідропероксіейкозатетраєнових кислот та ліпоксину А4 за умов ЦД відсутні. Було продемонстровано, що в судинах діабет не впливає на експресію білків потенціалзалежних калієвих каналів, але пригнічує відповідний струм. Експресія TRPМ-каналів судин легень зменшується за умов ЦД, але значно зростає їх активація, зумовлена активними формами кисню. Загалом гіперглікемія, резистентність до інсуліну, ендотеліальна дисфункція за умов ЦД можуть бути факторами, що призводять до змін легеневого кровообігу та можуть провокувати виникнення дисфункції легеневих судин.

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Pyridoxine, essential fatty acids, and protection against doxorubicin‐induced cardiotoxicity

Das

2024

J Biochem & Molecular Tox

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Sun et al. [1] showed that vitamin B6 (pyridoxine) protects against doxorubicin-(DOX) induced cardiotoxicity by its antioxidant and antiapoptotic actions principally by decreasing NHE1 (Na + /H + exchanger) expression and thus, improved DOX-induced cardiotoxicity. I would like to suggest an alternative explanation for the interesting results obtained.Data sharing is not applicable to this article as no new data were created or analyzed in this study.

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Arachidonic acid and lipoxin A4 attenuate alloxan‐induced cytotoxicity to RIN5F cells in vitro and type 1 diabetes mellitus in vivo

Abstract: AA seems to bring about its beneficial actions against alloxan-induced cytotoxicity and type 1 DM by enhancing the production of LXA4. © 2016 BioFactors, 43(2):251-271, 2017.

Cited by 73 publications

References 54 publications

Is There a Role for Bioactive Lipids in the Pathobiology of Diabetes Mellitus?

Is There a Role for Bioactive Lipids in the Pathobiology of Diabetes Mellitus?

Diabetes Mellitus and Pulmonary Circulation (Part 2)

Pyridoxine, essential fatty acids, and protection against doxorubicin‐induced cardiotoxicity

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