2020Food Production Processing and NutritionOpen access

Muscadine or amla extracts standardized to ellagic acid content ameliorate glucolipotoxicity associated β-cell dysfunction via inhibition of IL-1β and improved insulin secretion

Srikanth Earpina, Karen McDonough, Millicent Yeboah-Awudzi, Kristina J. Cook, Sita Aggarwal, Jack N. Losso

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Abstract

Abstract Glucolipotocixity induces IL-1 β secretion which impairs pancreatic β-cell insulin secretion. Ellagic acid and urolithin A have strong anti-inflammatory effect on cells. Muscadine and amla are very good sources of ellagic acid. The present study examined the effect of ellagic acid, ellagic acid-rich muscadine or amla extract, or urolothin A on inflammation in β cells under glucolipotoxic conditions. Rat NIT-1 β cells were incubated in glucolipotoxic conditions (33.3 mM glucose, 250 μM palmitic acid or 33.3 mM glucose + 250 μM palmitic acid with or without ellagic acid, ellagic acid-rich muscadine or amla extracts standardized to its ellagic acid content, or urolithin A). Inflammatory status was evidenced by ELISA analysis of insulin and IL-1β secretion. Ellagic acid-rich muscadine or amla extracts dose-dependently stimulated insulin secretion and down-regulated IL-1β better than pure ellagic acid, or urolithin A. Urolithin A did not statistically stimulate insulin secretion and did not inhibit IL-1β.

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Abstract Glucolipotocixity induces IL-1 β secretion which impairs pancreatic β-cell insulin secretion. Ellagic acid and urolithin A have strong anti-inflammatory effect on cells. Muscadine and amla are very good sources of ellagic acid. The present study examined the effect of ellagic acid, ellagic acid-rich muscadine or amla extract, or urolothin A on inflammation in β cells under glucolipotoxic conditions. Rat NIT-1 β cells were incubated in glucolipotoxic conditions (33.3 mM glucose, 250 μM palmitic acid or 33.3 mM glucose + 250 μM palmitic acid with or without ellagic acid, ellagic acid-rich muscadine or amla extracts standardized to its ellagic acid content, or urolithin A). Inflammatory status was evidenced by ELISA analysis of insulin and IL-1β secretion. Ellagic acid-rich muscadine or amla extracts dose-dependently stimulated insulin secretion and down-regulated IL-1β better than pure ellagic acid, or urolithin A. Urolithin A did not statistically stimulate insulin secretion and did not inhibit IL-1β.

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Available abstract

Abstract Glucolipotocixity induces IL-1 β secretion which impairs pancreatic β-cell insulin secretion. Ellagic acid and urolithin A have strong anti-inflammatory effect on cells. Muscadine and amla are very good sources of ellagic acid. The present study examined the effect of ellagic acid, ellagic acid-rich muscadine or amla extract, or urolothin A on inflammation in β cells under glucolipotoxic conditions. Rat NIT-1 β cells were incubated in glucolipotoxic conditions (33.3 mM glucose, 250 μM palmitic acid or 33.3 mM glucose + 250 μM palmitic acid with or without ellagic acid, ellagic acid-rich muscadine or amla extracts standardized to its ellagic acid content, or urolithin A). Inflammatory status was evidenced by ELISA analysis of insulin and IL-1β secretion. Ellagic acid-rich muscadine or amla extracts dose-dependently stimulated insulin secretion and down-regulated IL-1β better than pure ellagic acid, or urolithin A. Urolithin A did not statistically stimulate insulin secretion and did not inhibit IL-1β.

Key concepts: Ellagic acid, Palmitic acid, Secretion, Chemistry, Ellagitannin, Biochemistry, Fatty acid, Antioxidant

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Muscadine or amla extracts standardized to ellagic acid content ameliorate glucolipotoxicity associated β-cell dysfunction via inhibition of IL-1β and improved insulin secretion — Research Paper | ScholarLens