Quercetin has been included in the GLP-1 Diet factor formula firstly for its ability to inhibit the α-glucosidase and DPP-IV enzymes, which prolong the half-life of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).

Quercetin also shows a protective effect against metabolic dysfunction of glucose and lipids.

Studies have revealed that quercetin displays a wide range of pharmacological properties, including antihyperglycaemic effects. It can alleviate hyperglycaemia, hyperlipidemia, hypertension, and oxidative stress, contributing to lowering the risk of cardiovascular diseases emerging.

Quercetin decreases blood glucose levels, improves glucose tolerance, and enhances pancreatic β-cell function via various mechanistic pathways such as AMPK which regulates GLUT4 expression in adipose tissue and muscles.

It also regulates glycaemia by reducing GLUT2 expression and sodium-dependent glucose uptake in the gut, as well as lowering glucose absorption. It also inhibits the release of pro-inflammatory mediators, such as TNF-α, IL-1, -4, -6, and -8, preventing pancreatic β-cell damage.

Quercetin has been shown to improve insulin sensitivity, glucose metabolism, and insulin secretion in diabetic animal models by promoting pancreatic β-cell proliferation.

Due to its numerous benefits, quercetin has been identified to play a vital role in the treatment of Type 2 Diabetes Mellitus and in over weight individuals.

In our testing that is presented here support the conclusion that quercetin is a promising template for inclusion on weight management.

These would offer an alternative to current synthetic drugs that have undesirable side effects.

Quercetin is a flavonoid, present in various natural sources, which has demonstrated in vitro and in vivo antidiabetic properties. It improves oral glucose tolerance, as well as pancreatic β-cell function to secrete insulin. It inhibits the α-glucosidase and DPP-IV enzymes, which prolong the half-life of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).

Quercetin also inhibited carbohydrate digesting-enzymes (intestinal α-glucosidase and pancreatic α-amylase), reduced starch hydrolysis, decreased the rate of glucose absorption, as well as slowed down the progression of postprandial hyperglycaemia in in vitro settings as shown below:

Quercetin at a dose of 100 mg/day for 12 weeks reduced body fat and body mass index (BMI) of obese subjects.

The oral administration of multiple doses of quercetin decreased blood glucose and HbA1c levels, enhanced glycogen synthesis, decreased α-glucosidase activity, and insulin resistance.

In addition, it minimized β-cell insufficiency, enhancing pancreatic insulin secretion and controlling blood glucose levels in diabetic patients by reducing oxidative stress.

Due to its polyphenolic structure and its catechol moiety, quercetin displays antioxidant/radical scavenging properties These effects help to protect against the oxidative stress-induced damage to pancreatic β-cells associated with diabetes In addition, quercetin has cardioprotective, anti-tumour, anti-arthritis, and antimicrobial properties and it also prevents tyrosinase enzyme activity Quercetin has been reported to treat non-alcoholic fatty liver disease (NAFLD) by decreasing the level of liver enzymes, such as alanine transaminase (ALT) and aspartate transaminase (AST) oxidative stress, and inflammation, and by regenerating altered metabolites and gut microbiota. Quercetin has shown immunomodulatory activity, reducing the release of pro-inflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8, IL-4, and tumour necrosis factor (TNF)-α.

Pharmacological action of quercetin via different mechanistic pathways: Quercetin enhances pancreatic β-cell function and increases insulin release by inhibiting apoptosis, NF-κB, and JNK pathways; decreases glucose absorption in the kidney by inhibiting DPP-IV and COX-2 activity; decreases gluconeogenesis through inhibition of TNF-α and IL-4 in the liver; suppresses glucose reabsorption in the gastrointestinal tract by decreasing α-glucosidase activity; reduces blood glucose levels and oxidative stress by inhibiting IL-6 activity in the heart and blood vessels.

Quercetin inhibits fat accumulation in maturing human fat cells in culture, for example, while also suppressing the maturation of new fat cells and simultaneously triggering apoptosis (programmed destruction) in existing fat cells. Quercetin actually blocks the uptake of glucose from the blood, depriving fat cells of the raw material they need to manufacture and accumulate fat molecules.

In remarkable work published in mid-2008, the University of Georgia group found that while they could block fat cell production and enhance fat cell death dramatically using either quercetin or resveratrol (another powerful flavonoid) alone, when they used the two in combination they decreased lipid accumulation in cultured fat cells by nearly 70%, while increasing fat apoptosis by a whopping 310%!