Specific bioactive compounds in ginger and apple alleviate hyperglycemia in mice with high fat diet-induced obesity

Chethan Sampath1, Muhammed Raihan Rashid1, Shengmin Sang2

  • 1Department of Human Nutrition, College of Health Sciences, Qatar University, Qatar.

Food Chemistry
|March 4, 2017
PubMed

Insights

Phloretin from apples and [6]-gingerol from ginger reduce advanced glycation end-products (AGEs) and suppress the receptor for AGEs (RAGE) in mice. These natural compounds show potential for alleviating diabetes complications.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Nutritional Science

Background:

  • Prolonged hyperglycemia promotes advanced glycation end-product (AGE) formation, with N(ε)-(carboxymethyl)lysine (CML) elevated in diabetes.
  • Dicarbonyl compounds like methylglyoxal and glyoxal are key precursors to AGEs.

Purpose of the Study:

  • To investigate if phloretin and [6]-gingerol inhibit AGE formation and suppress the receptor for advanced glycation end products (RAGE) via the Nrf2 pathway.
  • To evaluate the efficacy of phloretin and [6]-gingerol in mitigating diabetes-induced complications in mice.

Main Methods:

  • C57BL/6 mice were fed a high-fat or standard diet for 17 weeks, supplemented with phloretin or [6]-gingerol at two doses.
  • Plasma glucose, insulin, AGEs, CML, liver enzymes, and oxidative stress markers (GSH/GSSG ratio, heme oxygenase-1, glyoxalase 1) were measured.

Main Results:

  • Phloretin and [6]-gingerol supplementation significantly reduced plasma glucose, insulin, AGEs, and liver enzymes.
  • Both compounds decreased AGEs and CML levels, enhancing the GSH/GSSG ratio, heme oxygenase-1, and glyoxalase 1 in liver tissue, indicating Nrf2 pathway activation.
  • The Nrf2-dependent pathway was implicated in the observed reduction of AGEs and RAGE suppression.

Conclusions:

  • Phloretin and [6]-gingerol demonstrate potential as dietary interventions to combat AGE formation and related diabetes complications.
  • These natural compounds may offer a therapeutic strategy by modulating the Nrf2 pathway and reducing oxidative stress in diabetes.

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