While Type I diabetes is an autoimmune disease which results into pancreatic beta cell death and resultant lack of Insulin production, Type II diabetes is scientifically most challenging disease, which is characterized by elevated insulin resistance and glucose intolerance. Type II diabetes can occur as a result of dysfunction in glucose, lipid and energy homeostasis in any or all of the following organs/organ systems including liver, adipose, muscle, gastrointestinal (GI) tract. Elevated levels of serum glucose and free fatty acids occurring due to imbalances in lipid and carbohydrate metabolism then leads to endoplasmic reticular stress in pancreatic beta cells, leading ultimately to pancreatic beta cell death (terminal diabetes).
Knowledge-base on diabetes/dyslipidemia and metabolic syndrome through basic research.
Improving Insulin sensitivity/ glucose tolerance
Reduction in serum glucose
Improvement of circulating lipid profile
Anti-diabetic/dyslipidemic molecules by target based drug designs and synthesis:
Natural product as a source of biologically active Anti-diabetic/dyslipidemic molecules (marine/terrestrial).
Studies on functional regulation of carbohydrate and lipid metabolism by metabolic nuclear receptors.
Proteomic analysis of 3T3L-1 cells treated with adipogenic compounds
Studies on pancreatic ER stress.
CDR-134D123 (anti-hyperglycemic, Phase I): Natural product
CDR134F194: IND filed
Puffer fish oil: IND filed.
8 lead compounds identified with anti-hyperglycemic and/oranti-dyslipidemic activities
Development and optimization of proteomic approaches for proteomic profiling of lead compound treated
Development and optimization of screening systems for metabolic nuclear receptors
Development of pancreatic islet cell culture for ER stress studies