Researchers at the Madras Diabetic Research foundation and Dr. Mohans Diabetes Specialities centre, Chennai, India have established a link between Diabetes and adipocytes(fat cells) in our body. Under induced oxidative stress fat cells switch over to a senile (aged) phenotype characterised by increase in generation of Reactive Oxygen Species (ROS), DNA damage and shortened telomeres. Finny Monickaraj et al. point out that it is the switch of these stressed fat cells to a senile phenotype that leads to glucose uptake impairment, thus insulin resistance.
Off late, the role of adipose tissue is not only being implicated in energy storage but also in longevity, inflammation, metabolic dysfunction and genesis of age related disorders. Experiments carried out in animal models indicate that an excess of fat cells impels onset of metabolic dysfunction. In obese conditions (state of aging) adipocytes secrete pro-inflammatory cytokines which make the cell micro-environment deleterious leading to inflammation and insulin resistance. This implies that metabolic disorders like diabetes are in harmony with the aging process. Aging of cells, is thus a critical contributing factor in metabolic imbalance.
Adipocyte cells were treated with hydrogen peroxide (H2O2) externally, glucose oxidase to generate H2O2 in-situ, asymmetric NG, NG-dimethylarginine (ADMA) and fluctuating glucose concentrations (to mimic diabetic conditions) for a fortnight. The cells were then assayed for molecular changes due to the induced oxidative stress. Researchers found a substantial increase in ROS in cells that were treated compared to the control cells. This increase could also be the reason for DNA damage and shortening of telomere length. Besides up-regulation of p53, p21 and TNFα (senescent proteins), adiponectin, a protein responsible for glucose regulation and fatty acid breakdown, was found to be down-regulated. Insulin stimulated 2‑deoxyglucose uptake in stressed cells compared to the control appeared to be low, giving a clear connection between fat cells and insulin resistance in the body.
Research done by Finny Monickaraj et al. has expanded our knowledge in the field of diabetes. However detailed studies are required to prevent insulin resistance arising from fat cell signalling. There is an indispensable need to further study the molecular mechanisms that determine alteration of fat cell function due to oxidative stress. These studies can lead us to the cause of many age-related disorders that are still muffled.