Pterostilbene (PTE) (3-5 dimethoxy-4-hydroxy-trans-stilbenes) is an analogue of resveratrol. It is extracted and isolated from a natural source of the heartwood of Pterocarpus marsupium Roxb., red grape skin, and blueberries (Vaccinium spp.). Substantial evidence suggested that PTE displayed numerous preventive and therapeutic properties in many metabolic disorders such as diabetes and obesity. Metabolic diseases result in Insulin resistance (IR) which advances to impaired sensitivity to insulin-mediated glucose disposal. The prominent role of SIRT (silent information regulator proteins) is now getting emphasized in metabolic disorders. SIRT1 represses Uncoupling protein 2 (UCP2) expressions which are further responsible for improving synthesis of ATP from glucose. This results in improving glucose utilization and insulin secretion, thus preventing IR. SIRT1 also exhibits prominent role in facilitating fatty acid mobilization thereby inhibiting adiposity. Metabolic disorders are therefore the consequences of SIRT1 downregulation. Pterostilbene, being a SIRT1 activator, increases insulin sensitivity reduces adiposity, therefore can prove to be beneficial in diabetes as well as obesity. The review summarizes therapeutic effects portrayed by Pterostilbene via the SIRT1 pathway in metabolic diseases.

Telomeres are natural nucleoprotein structures that cover the ends of chromosomes. The phenomenon of telomere shortening, which plays a crucial role in maintaining the stability of the genome, occurs gradually over time when cells undergo division due to the end replication issue. Multiple studies have demonstrated a correlation between telomere shortening and a range of illnesses, including diabetes, dyslipidemia, cardiovascular disease, cancer, and mortality. Diet and lifestyle can affect telomere length. There exists a beneficial association between telomere length and the Mediterranean diet, particularly with regards to the consumption of dietary fiber derived from whole grains and vegetables. Micronutrients such as vitamins and trace elements also play a role in cell metabolism.  Some micronutrients, such as vitamin D, folate, and vitamin B12, are associated with telomere biology and cellular aging. Vitamin B12 is essential for DNA synthesis and epigenetic methylation processes. The present systematic review examines the results from clinical trials conducted in humans evaluating the role of vitamin B12 on telomere length. Cellular senescence is a state characterized by inflammation, altered cellular metabolism, genomic instability, and telomere dysfunction, which can be induced by changes in methylation patterns and oxidative stress. Vitamin B12 maintains antioxidative defense. Through these pathways, sufficient amounts of vitamin B12 may potentially play a role in the restoration of DNA damage. Most of the evidence is based on very few randomized clinical trials. Therefore, more extensive prospective cohort studies and better-designed randomized clinical trials are required to validate the correlations outlined in this review.

Telomeres are natural nucleoprotein structures that cover the ends of chromosomes. The phenomenon of telomere shortening, which plays a crucial role in maintaining the stability of the genome, occurs gradually over time when cells undergo division due to the end replication issue. Multiple studies have demonstrated a correlation between telomere shortening and a range of illnesses, including diabetes, dyslipidemia, cardiovascular disease, cancer, and mortality. Diet and lifestyle can affect telomere length. There exists a beneficial association between telomere length and the Mediterranean diet, particularly with regards to the consumption of dietary fiber derived from whole grains and vegetables. Micronutrients such as vitamins and trace elements also play a role in cell metabolism.  Some micronutrients, such as vitamin D, folate, and vitamin B12, are associated with telomere biology and cellular aging. Vitamin B12 is essential for DNA synthesis and epigenetic methylation processes. The present systematic review examines the results from clinical trials conducted in humans evaluating the role of vitamin B12 on telomere length. Cellular senescence is a state characterized by inflammation, altered cellular metabolism, genomic instability, and telomere dysfunction, which can be induced by changes in methylation patterns and oxidative stress. Vitamin B12 maintains antioxidative defense. Through these pathways, sufficient amounts of vitamin B12 may potentially play a role in the restoration of DNA damage. Most of the evidence is based on very few randomized clinical trials. Therefore, more extensive prospective cohort studies and better-designed randomized clinical trials are required to validate the correlations outlined in this review.