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Mumefural prevents insulin resistance and amyloid-beta accumulation in the brain by improving lowered interstitial fluid pH in type 2 diabetes mellitus

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BIOMEDICAL RESEARCH-TOKYO
卷 44, 期 1, 页码 17-29

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BIOMEDICAL RESEARCH PRESS LTD
DOI: 10.2220/biomedres.44.17

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The study aimed to investigate the potential of mumefural in preventing hyperglycemia, a typical symptom of type 2 diabetes mellitus (T2DM). Using OLETF rats as a T2DM model, it was found that mumefural reduced hyperglycemia, insulin resistance, and plasma triglyceride concentration. Mumefural also increased protein expression of SMCT1 in the colon and elevated interstitial fluid pH around the brain hippocampus, leading to a decrease in amyloid-beta accumulation.
The present study tried to clarify if mumefural would prevent hyperglycemia, one of the typical symptoms of type 2 diabetes mellitus (T2DM), since mumefural is an extract from Japanese apricots preventing hyperglycemia. To clarify if mumefural would prevent T2DM pathogenesis, we used Otsuka Long-Evans Tokushima fatty (OLETF) rats, T2DM model. Mumefural diminished hyperglycemia, HOMA-IR and plasma triglyceride concentration in OLETF rats under fasting conditions. In addition, mumefural elevated protein expression of sodium-coupled monocarboxylate transporter 1 (SMCT1) in the distal colon participating in absorption of weak organic acids, which behave as bases but not acids after absorption into the body. Mumefural also increased the interstitial fluid pH around the brain hippocampus lowered in OLETF rats compared with non-T2DM LETO rats used as control for OLETF rats. Amyloid-beta accumulation in the brain decreased in accordance with the pH elevation. On the one hand, mumefural didn't affect plasma concentrations of glucagon, GLP-1, GIP or PYY under fasting conditions. Taken together, these observations indicate that: 1) mumefural would be a useful functional food improving hyperglycemia, insulin resistance and the lowered interstitial fluid pH in T2DM; 2) the interstitial fluid pH would be one of key factors influencing the accumulation of amyloid-beta.

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