Nutraceuticals and Supplements in Management of Prediabetes and Diabetes

Abstract

Dysglycemia is a condition preceding diabetes mellitus. The two situations inherent in this condition are called impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). If one of these situations is found in the patient, after the advice of an appropriate diet and physical activity, the addition of nutraceuticals or supplements can be considered, which can stop or delay the progression to diabetes mellitus over time. The purpose was to compile a systematic review about the use of nutraceuticals for treating diabetes and prediabetes and to offer a valuable resource for colleagues working on this crucial subject, thereby improving patient health. The added value of the paper compared to other reviews is that it was written by experts appointed by five different scientific societies dealing with diabetes, nutrition, and complications.

Keywords: Dysglycemia; diabetes; nutraceuticals; prediabetes; supplements.

Figure 1

Mechanisms of action of Ascophyllum nodosum and Fucus vesiculosus hypoglycemic activity. ACC: acetyl-CoA carboxylase; Akt: serine/threonine kinase; AMPK: adenosine monophosphate-activated protein kinase; G6Pase: glucose-6-phosphatase; GLUT: glucose transporter; PEPCK: phosphoenolpyruvate carboxykinase. : decrease; : increase.

Figure 2

Hypoglycemic mechanisms of action of Lagerstroemia speciose. PPAR-α/γ: peroxisome proliferator-activated receptor-α/γ. : decrease; : increase.

Figure 3

Hypoglycemic mechanisms of action of Berberis. AMPK: adenosine monophosphate-activated protein kinase; G6Pase: glucose-6-phosphatase; PEPCK: phosphoenolpyruvate carboxykinase. : decrease; : increase.

Figure 4

Glucose-lowering mechanisms of action of Cinnamomum. Akt: serine/threonine kinase; GLUT: glucose transporter; IR: insulin receptor; IRS-1/2: insulin receptor substrate type 1/2; PI3K: phosphatidylinositol 3-kinase; PPAR-α/γ: peroxisome proliferator-activated receptor-α/γ. : increase.

Figure 5

Hypoglycemic mechanisms of action of Gymnema sylvestre.

Figure 6

Glucose-lowering mechanisms of action of Ilex paraguariensis. AMPK, adenosine monophosphate-activated protein kinase; GLUT, glucose transporter; , decrease; , increase.

Figure 7

Glucose-lowering mechanisms of action of Momordica charantia. AMPK: adenosine monophosphate-activated protein kinase; GLUT: glucose transporter; G6Pase: glucose-6-phosphatase; PEPCK: phosphoenolpyruvate carboxykinase. : decrease; : increase.

Figure 8

Hypoglycemic mechanisms of action of Morus. G6Pase: glucose-6-phosphatase; GLUT: glucose transporter; GK: glucokinase, PEPCK: phosphoenolpyruvate carboxykinase; PFK: phosphofructokinase, PK: pyruvate kinase; SGLT1: sodium glucose co-transporter 1; PI3K/AKT: phosphatidylinositol 3-kinase/serine/threonine kinase. : decrease; : increase.

Figure 9

Potential hypoglycemic mechanisms of action of Olea europaea. AGEs; advanced glycation end-products; GLP-1: glucagon-like peptide-1. : decrease; : increase.

Figure 10

Possible mechanisms of action for alpha-lipoic acid in glycemic control. AKT: serine/threonine kinase; AMPK: adenosine monophosphate-activated protein kinase; GLUT4: glucose transporter; IRS-1: insulin receptor substrate type 1; MAPK: mitogen-activated protein kinase; PI3K: phosphatidylinositol 3-kinase. : increase.

Figure 11

Potential hypoglycemic mechanisms of action of Omega-3. : decrease; : increase.

Figure 12

Possible mechanisms of action for essential amino acids in glycemic homeostasis. ATP: adenosine triphosphate; CCK: cholecystokinin; GIP: glucose-dependent insulinotropic peptide; GLP-1: glucagon-like peptide-1; PYY: peptide tyrosine–tyrosine; mTORC1: mammalian target of rapamycin complex 1.