4.7 Article

Long-term kappa-carrageenan consumption leads to moderate metabolic disorder by blocking insulin binding

期刊

PHARMACOLOGICAL RESEARCH
卷 165, 期 -, 页码 -

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2020.105417

关键词

kappa-Carrageenan; Glucose metabolism; Insulin receptor; Receptor binding; Diabetes

资金

  1. National Key R&D Program of China [2018YFD0901103]
  2. Natural Science Foundation of Zhejiang [LY18C190004, LY19H030001, LQ20D060001]
  3. NSFC [31872540]
  4. China Agriculture Research System [CARS-50]
  5. Ningbo Programs for Science and Technology Development [2019C50095]
  6. Medical Science and Technology of Zhejiang province [2018KY726, 2018KY710]
  7. K.C. Wong Magna Fund in Ningbo University

向作者/读者索取更多资源

The study showed that carrageenan reduced weight gain in mice without affecting food intake, but impaired glucose metabolism by interfering with insulin binding to receptors, affecting insulin sensitivity, inhibiting the insulin PI3K/AKT signaling pathway, and causing non-diabetic weight gain reduction.
Carrageenan (CGN) is a common food additive, and questions have been raised regarding its safety for human consumption. The purpose of this study was to investigate the impact of kappa-CGN on glucose intolerance and insulin resistance from the perspective that kappa-CGN may interfere with insulin receptor function and affect insulin sensitivity and signaling, thereby leading to body weight loss. The health effects of kappa-CGN on C57BL/6 mice were assessed over a 90-d period by monitoring changes in body weight, glucose tolerance, insulin tolerance, fasting glucose and insulin levels, and expression of insulin-pathway-related proteins. Furthermore, HepG2 cells were used to detect the binding of kappa-CGN on insulin receptor and measure its effect on downstream signal transduction. In mice, kappa-CGN treatment reduced weight gain without affecting food intake. Glucose and insulin tolerance tests revealed that kappa-CGN treatment increased blood glucose levels and glycosylated hemoglobin levels, while hepatic and muscle glycogen levels were decreased, suggesting that kappa-CGN affected glucose metabolism in mice. Interestingly, kappa-CGN treatment did not cause typical diabetic symptoms in mice, as indicated by low levels of fasting and postprandial blood glucose, in addition to normal pancreatic tissue and insulin secretion. The binding studies revealed that kappa-CGN could competitively bind to the insulin receptor with FITC-insulin and thereby disrupt PI3K and Akt activation, thus suppressing expression of glucose transporters and glycogen synthase. In summary, this study revealed that kappa-CGN reduced weight gain without affecting food intake, but impaired glucose metabolism in mice by interfering with insulin binding to receptors, thereby affecting the sensitivity of insulin and inhibiting the insulin PI3K/AKT signaling pathway, causing non-diabetic weight gain reduction.

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