Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Russell 2020 Nutrients

From Bioblast
Revision as of 17:50, 18 September 2020 by Plangger Mario (talk | contribs) (Created page with "{{Publication |title=Russell JS, Griffith TA, Naghipour S, Vider J, Du Toit EF, Patel HH, Peart JN, Headrick JP (2020) Dietary ฮฑ-linolenic acid counters cardioprotective dysf...")
(diff) โ† Older revision | Latest revision (diff) | Newer revision โ†’ (diff)
Publications in the MiPMap
Russell JS, Griffith TA, Naghipour S, Vider J, Du Toit EF, Patel HH, Peart JN, Headrick JP (2020) Dietary ฮฑ-linolenic acid counters cardioprotective dysfunction in diabetic mice: unconventional PUFA protection. Nutrients 12:E2679.

ยป PMID: 32887376 Open Access

Russell JS, Griffith TA, Naghipour S, Vider J, Du Toit EF, Patel HH, Peart JN, Headrick JP (2020) Nutrients

Abstract: Whether dietary omega-3 (n-3) polyunsaturated fatty acid (PUFA) confers cardiac benefit in cardiometabolic disorders is unclear. We test whether dietary -linolenic acid (ALA) enhances myocardial resistance to ischemia-reperfusion (I-R) and responses to ischemic preconditioning (IPC) in type 2 diabetes (T2D); and involvement of conventional PUFA-dependent mechanisms (caveolins/cavins, kinase signaling, mitochondrial function, and inflammation). Eight-week male C57Bl/6 mice received streptozotocin (75 mg/kg) and 21 weeks high-fat/high-carbohydrate feeding. Half received ALA over six weeks. Responses to I-R/IPC were assessed in perfused hearts. Localization and expression of caveolins/cavins, protein kinase B (AKT), and glycogen synthase kinase-3 ฮฒ (GSK3ฮฒ); mitochondrial function; and inflammatory mediators were assessed. ALA reduced circulating leptin, without affecting body weight, glycemic dysfunction, or cholesterol. While I-R tolerance was unaltered, paradoxical injury with IPC was reversed to cardioprotection with ALA. However, post-ischemic apoptosis (nucleosome content) appeared unchanged. Benefit was not associated with shifts in localization or expression of caveolins/cavins, p-AKT, p-GSK3ฮฒ, or mitochondrial function. Despite mixed inflammatory mediator changes, tumor necrosis factor-a (TNF-a) was markedly reduced. Data collectively reveal a novel impact of ALA on cardioprotective dysfunction in T2D mice, unrelated to caveolins/cavins, mitochondrial, or stress kinase modulation. Although evidence suggests inflammatory involvement, the basis of this "un-conventional" protection remains to be identified.

โ€ข Bioblast editor: Plangger M


Labels: MiParea: Respiration 





HRR: Oxygraph-2k 

2020-09