31 March 2010 | Kati Hanhineva, Riitta Törrönen, Isabel Bondia-Pons, Jenna Pekkinen, Marjukka Kolehmainen, Hannu Mykkänen and Kaisa Poutanen
Dietary polyphenols, including flavonoids, phenolic acids, proanthocyanidins, and resveratrol, are phytochemicals found in plant-based foods that may influence carbohydrate metabolism. Animal studies and limited human trials suggest that polyphenols can reduce postprandial glycemic responses, improve insulin secretion, and enhance insulin sensitivity. Mechanisms include inhibiting carbohydrate digestion and glucose absorption, stimulating insulin secretion, modulating glucose release from the liver, and activating insulin receptors. Polyphenols also modulate intracellular signaling pathways and gene expression, supporting their role in glucose homeostasis. Epidemiological evidence supports these findings, but more clinical studies are needed to confirm their benefits in preventing insulin resistance and type 2 diabetes.
Polyphenols affect carbohydrate digestion and glucose absorption in the intestine by inhibiting α-amylase and α-glucosidase, reducing glucose absorption. They also influence glucose transporters, such as SGLT1 and GLUT2, which are critical for intestinal glucose uptake. Studies show that polyphenols like chlorogenic acid, quercetin, and tea catechins inhibit glucose transport, leading to delayed glycemic responses. In human studies, polyphenol-rich foods like apple juice, red wine, and berries improve short-term glycemic control. However, more research is needed to confirm their long-term benefits.
Polyphenols also influence pancreatic β-cell function by enhancing insulin secretion, improving insulin sensitivity, and protecting β-cells from damage. In vitro and in vivo studies show that compounds like genistein, EGCG, and rutin improve β-cell function and insulin release. These effects are mediated through various mechanisms, including modulation of intracellular signaling pathways and Ca²⁺ signaling. However, the exact mechanisms remain unclear.
Polyphenols stimulate glucose uptake in insulin-sensitive and non-insulin-sensitive tissues by activating glucose transporters like GLUT4. They enhance insulin-stimulated glucose uptake through pathways involving AMPK and PI3K. Studies show that compounds like resveratrol, aspalathin, and kaempferol improve glucose uptake in muscle and adipose tissues. However, the effects vary depending on the compound and the tissue type.
Polyphenols also influence liver function by modulating glucose metabolism. The liver plays a key role in maintaining glucose homeostasis by storing glucose as glycogen and producing glucose through glycogenesis and gluconeogenesis. Polyphenols may enhance liver glucose metabolism by modulating key enzymes involved in these processes. However, the exact mechanisms require further investigation.
In conclusion, dietary polyphenols have potential to improve glucose homeostasis by influencing carbohydrate digestion, insulin secretion, β-cell function, and glucose uptake. However, more clinical studies are needed to confirm their long-term benefits in preventing metabolic disorders.Dietary polyphenols, including flavonoids, phenolic acids, proanthocyanidins, and resveratrol, are phytochemicals found in plant-based foods that may influence carbohydrate metabolism. Animal studies and limited human trials suggest that polyphenols can reduce postprandial glycemic responses, improve insulin secretion, and enhance insulin sensitivity. Mechanisms include inhibiting carbohydrate digestion and glucose absorption, stimulating insulin secretion, modulating glucose release from the liver, and activating insulin receptors. Polyphenols also modulate intracellular signaling pathways and gene expression, supporting their role in glucose homeostasis. Epidemiological evidence supports these findings, but more clinical studies are needed to confirm their benefits in preventing insulin resistance and type 2 diabetes.
Polyphenols affect carbohydrate digestion and glucose absorption in the intestine by inhibiting α-amylase and α-glucosidase, reducing glucose absorption. They also influence glucose transporters, such as SGLT1 and GLUT2, which are critical for intestinal glucose uptake. Studies show that polyphenols like chlorogenic acid, quercetin, and tea catechins inhibit glucose transport, leading to delayed glycemic responses. In human studies, polyphenol-rich foods like apple juice, red wine, and berries improve short-term glycemic control. However, more research is needed to confirm their long-term benefits.
Polyphenols also influence pancreatic β-cell function by enhancing insulin secretion, improving insulin sensitivity, and protecting β-cells from damage. In vitro and in vivo studies show that compounds like genistein, EGCG, and rutin improve β-cell function and insulin release. These effects are mediated through various mechanisms, including modulation of intracellular signaling pathways and Ca²⁺ signaling. However, the exact mechanisms remain unclear.
Polyphenols stimulate glucose uptake in insulin-sensitive and non-insulin-sensitive tissues by activating glucose transporters like GLUT4. They enhance insulin-stimulated glucose uptake through pathways involving AMPK and PI3K. Studies show that compounds like resveratrol, aspalathin, and kaempferol improve glucose uptake in muscle and adipose tissues. However, the effects vary depending on the compound and the tissue type.
Polyphenols also influence liver function by modulating glucose metabolism. The liver plays a key role in maintaining glucose homeostasis by storing glucose as glycogen and producing glucose through glycogenesis and gluconeogenesis. Polyphenols may enhance liver glucose metabolism by modulating key enzymes involved in these processes. However, the exact mechanisms require further investigation.
In conclusion, dietary polyphenols have potential to improve glucose homeostasis by influencing carbohydrate digestion, insulin secretion, β-cell function, and glucose uptake. However, more clinical studies are needed to confirm their long-term benefits in preventing metabolic disorders.