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Spherix Announces Post-Hoc Analysis of Phase 3 Trial With D-Tagatose in Diabetes
Date:12/2/2010

acid transport mediated by GLUT-4. This negative feedback mechanism may protect adipocytes from lipid overload and restrict further expansion of adipose tissue, which leads to obesity and metabolic complications. However, when the negative feedback mechanism is activated, fatty acid transport in the enlarged cells is inhibited, and the enlarged cells are in a sense no longer available to participate in glucose homeostasis.

The association between high carbohydrate diet and hypertriglyceridemia is stronger for those who are overweight (BMI >28). Insulin resistance is more common among the overweight and the obese (BMI >30) and is suspected to be a result of carbohydrate-induced hypertriglyceridemia. [Parks, 2002]  In the adipocyte, glucose is transported into the cell mediated by the glucose transporter type-4 (GLUT-4). Glucose can be converted to alpha-glycerol phosphate, the main source of the glycerol backbone of triglycerides. These triglycerides, during adipocyte dysfunction, are broken down and released back into circulation resulting in free fatty acid overload at skeletal muscle and insulin resistance [Guilherme, 2008].

It is hypothesized that reducing glucose transport into the adipocyte could decrease triglyceride deposition, thus making less triglyceride available for release during a metabolically dys-regulated state. D-tagatose shares common metabolic pathways with other sugars and it is possible that it may compete with glucose for transport into the adipocytes via the GLUT-4 transporter. Once in the cell, it may interfere with lipolysis of the formed triglycerides. If this occurred, D-tagatose would be most effective in those patients whose diabetes control was impaired (resulting in high HbA1c levels) to a larger extent by metabolic dysregulation of the adipocytes.

As a result of this analysis of the Phase 3 clinical trial results, Biospherics is currently designing new studies in cell culture, animal models and
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SOURCE Spherix Incorporated
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