It also affects triglyceride synthesis (via the increase in glycerol and acyl portions of the triglyceride molecules from fructose catabolism). This disturbance to metabolism may be related to insulin resistance commonly observed in high fructose diets.

Fructose, of course, does not stimulate insulin secretion from pancreatic beta cells, therefore consumption of fructose-containing foods produce smaller postprandial insulin response than the consumption of glucose-containing foods. The production of leptin is regulated by the insulin response to meals, so fructose also reduces the concentrations of circulating leptin. Both plasma insulin and leptin are involved in the regulation of body adiposity by inhibiting food intake and increasing energy expenditure — acting in the central nervous system in long-term regulation of energy homeostasis.

Increased Nonesterified fatty acid concentrations mediate changes in relationships between insulin resistance, increased fasting insulin concentrations, glucose intolerance and increased triglycerides. These elevated concentrations are a result of chronic imbalance between energy intake an output and increased body adiposity. It therefore follows that an increase in fructose consumption — leading to an increase in body weight because of decreased insulin secretion and reduced leptin producion, may well result in an increase in nonesterified fatty acids.

Fructose — (fruit sugar) — during digestion it is produced along with glucose, It is the sweetest of sugars, found in ripe fruit, vegetables, honey and corn syrup.