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Taurine supplementation restores pancreatic and mesenteric endothelial function in protein malnourished mice
Author(s) -
Davel Ana Paula,
Carneiro Everardo Magalhães,
Vettorazzi Jean,
Guizoni Daniele Mendes
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.696.23
Subject(s) - taurine , endocrinology , medicine , myograph , mesenteric arteries , vasodilation , endothelial dysfunction , nitric oxide , endothelium , vasoconstriction , electrical impedance myography , artery , chemistry , biochemistry , amino acid
Protein malnutrition predisposes to type 2 diabetes and hypertension. Reduced endothelium‐mediated vasodilation is a risk factor for cardiometabolic disorders, increasing vascular resistance and impairing pancreatic islet blood flow and insulin secretion. Therefore, restoring endothelial function could be relevant for malnourished individuals. Diet supplementation with taurine has been reported to be an antihypertensive and vasculoprotective therapy. In the present study we evaluated the effects of taurine supplementation on the protein restriction‐induced vasodilator endothelial dysfunction in two different vascular beds: small mesenteric arteries, that contribute for total vascular resistance, and intralobular pancreatic artery, responsible for pancreatic blood flow. For this, male post‐weaned mice fed a normal‐ (14%, NP) or an isocaloric low‐protein (6%, LP) diet for 90 days. Concomitantly, half of the LP mice received 2.5% taurine supplementation in drinking water. Blood pressure (BP) was higher in LP mice when compared to NP, which was reversed by taurine supplementation. Vascular function was evaluated by using a wire myograph and no changes in vessel internal diameter among groups were found. The endothelium‐dependent relaxation to acetylcholine (ACh) was significantly reduced by LP diet and normalized by taurine supplementation in both mesenteric and pancreatic arteries. Next, we investigated the involvement of nitric oxide synthase (NOS)‐derived NO and the endothelium derived‐hyperpolarization (EDH) by incubating the vessels with L‐NAME and 20 mM KCl, respectively. L‐NAME reduced the relaxation to ACh in both arteries. However, L‐NAME abolished differences among groups only in mesenteric arteries, suggesting a role for NOS‐derived NO in the LP‐induced endothelial dysfunction in the mesenteric bed. In intralobular pancreatic arteries, LP diet‐induced endothelial dysfunction was associated with reduced EDH. Taurine supplementation reversed the impaired NOS and EDH contribution to ACh‐induced relaxation. The relaxation to sodium nitroprusside was not modified by LP diet or taurine, suggesting no changes in vascular smooth muscle responsiveness. In conclusion, our data revealed that post‐weaning protein restriction induces endothelial dysfunction in mesenteric and pancreatic arteries by different pathways: in resistance mesenteric arteries results in impaired NOS‐derived NO, while in pancreatic vessels there is an impair in EDH. Interestingly, diet supplementation with taurine restores the endothelial function in both mesenteric and pancreatic vessels and reduces BP in protein‐restricted mice. Therefore, taurine emerges as a potential therapy for vascular dysfunction associated with malnutrition. Support or Funding Information São Paulo Research Foundation‐FAPESP This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .