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

cytes in the body [van Harmelen, 2003]. Adipose tissue has an important role in the control of glucose homeostasis. When fatty acid and triglyceride metabolism in adipocytes is altered by obesity, primary insulin resistance in skeletal muscle can occur [Guilherme, 2008]. Impaired responsiveness of skeletal muscle to insulin is a precondition for the onset of Type 2 diabetes. Literature has documented the probable causal relationship between weight gain and decreasing insulin sensitivity and weight loss and increasing insulin sensitivity [Parks, 2002]. Therefore, adipocytes have been hypothesized to be a contributing factor to the insulin response to plasma glucose.

Adipocytes synthesize and store triglycerides during feeding as well as release fatty acids, transported in the blood as triglycerides during fasting. In the normal homeostatic state, the balance of triglyceride storage and lipolysis is maintained at a rate appropriate to the caloric intake. During a disruption of the normal metabolic and secretory function of the adipocyte, for example in the overweight (high BMI) diabetic individual, a prolonged caloric surplus contributes to a lipid excess, enhanced lipolysis and consequent overload of free fatty acids in the skeletal muscle and liver contributing to decreased insulin sensitivity [Guilherme, 2008].

The significance of adipose tissue in regulating whole-body metabolism by sequestering lipid is demonstrated in the literature [Sovik, 1996] [Moitra, 1998] [Laustsen, 2002] [Shimomura, 1998]. The physical size of the adipocytes affects their function as well. Subcutaneous adipocytes have been reported to be heterogeneous in size and intrinsic insulin sensitivity [Varlamov, 2010]. Smaller adipocytes normally respond to insulin by increasing lipid uptake, but adipocytes with cell diameters larger than 80-100 micrometers are insulin resistant. It appears that, when cell size approaches a critical boundary, adipocytes lose insulin-dependent fatty
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