Abstract
Diabetes mellitus (DM) represents a group of metabolic disorders that leads to acute and long-term serious complications and is considered a worldwide sanitary emergence. Type 2 diabetes (T2D) represents about 90% of all cases of diabetes, and even if several drugs are actually available for its treatment, in the long term, they show limited effectiveness. Most traditional drugs are designed to act on a specific biological target, but the complexity of the current pathologies has demonstrated that molecules hitting more than one target may be safer and more effective. The purpose of this review is to shed light on the natural compounds known as α-glucosidase and Protein Tyrosine Phosphatase 1B (PTP1B) dual-inhibitors that could be used as lead compounds to generate new multitarget antidiabetic drugs for treatment of T2D.
Highlights
Type 2 diabetes is a complex pathology characterized by hyperglycemia and metabolic abnormalities affecting different organs and tissues, such as liver, muscle, adipose tissue, and pancreas
These drugs include: inhibitors of intestinal α-glucosidases, which delay intestinal absorption of glucose; metformin, which blocks hepatic gluconeogenesis; different types of secretagogues that stimulate the release of insulin from pancreatic β-cells; thiazolidinediones, which stimulate the storage of circulating fatty acids into adipocytes, thereby improving insulin sensitivity in several peripheral tissues; and the sodium/glucose cotransporter 2 (SGLT-2)
Studies conducted on extracts obtained from Hizikia fusiformis (Harvey) Okamura lead to identification of several fatty acids (92, 93, 96–98) as natural α-glucosidase and Protein Tyrosine Phosphatase 1B (PTP1B)
Summary
Type 2 diabetes is a complex pathology characterized by hyperglycemia and metabolic abnormalities affecting different organs and tissues, such as liver, muscle, adipose tissue, and pancreas. Subjects affected by T2D can rely on several oral antihyperglycemic drugs showing different mechanisms of action to keep glycaemia under control These drugs include: inhibitors of intestinal α-glucosidases, which delay intestinal absorption of glucose; metformin, which blocks hepatic gluconeogenesis; different types of secretagogues that stimulate the release of insulin from pancreatic β-cells; thiazolidinediones, which stimulate the storage of circulating fatty acids into adipocytes, thereby improving insulin sensitivity in several peripheral tissues; and the sodium/glucose cotransporter 2 (SGLT-2). The failure of mono-drug therapy is mainly due to the inability of such drugs to replace physiological functions of insulin Even if these drugs are able to compensate a specific metabolic defect, they unexpectedly induce severe unbalance in other metabolic pathways.
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