Acarbose improves health and lifespan in aging HET3 mice
Acarbose is a pseudotetrasaccharide of microbial origin that inhibits intestinal alpha-glucosidases, i.e. it dose-dependently delays the digestion of disaccharides, oligosaccharides, and polysaccharides. The derived glucose is released and passes into the blood more slowly, reducing and delaying the postprandial glucose increase. Therefore, it is used for treatment (with a diet alone or in combination with a diet and other medications) to treat type 2 diabetes.
In addition, this drug can prevent the development of complications resulting from untreated type 2 diabetes, such as heart attack, stroke, or other related complications, such as renal impairment, nerve damage, and eye problems, including damage to or loss of eyesight, or gum disease.
Apparently, there are some longevity genes that may allow us to reach our potential life limit, which is approximately 115 years, with a more than the acceptable quality of life. These genes are being investigated as possible therapeutic targets; some of them are CETP, APOC3, and IGF-1R (genes related to glucose metabolism).
Drugs based solely on molecular targets are already being developed. In fact, some drugs are already approved for human use (metformin, acarbose), others are available but need improvement (such as rapamycin and the senolytics) and others can be developed conventionally.
As we can see, acarbose is one of those drugs in which there is much hope for extending our life. This is because acarbose has important effects on glucose metabolism, which may influence various processes that accelerate the aging of the organism.
According to several studies in mice, acarbose improves inflammatory markers and reduces cardiovascular events. Consequently, it may influence the fundamental processes that contribute to age-related diseases, which, after all, are the main cause of mortality.
It is not known with certainty which molecular or cellular mechanism is predominantly responsible for the chronic disease risk associations with elevated glucose. Some casual mechanisms, such as inappropriate glycosylation events that lead to accelerated aging, can cause impair cellular functions from DNA repair.
“Thus by indirect means, changes in glucose levels could significantly impact transcriptional programs or hormonal signaling to coordinately regulate processes currently known (or unknown) to influence the aging process”
All of the research confirms the hope placed in acarbose and prompts further attention to the effects of transient periods of high blood glucose on aging and diseases of aging, including cancer, and should motivate studies of acarbose and other drugs for glucose control in humans.