fructose - Fructose,unlikeglucose, cells(40,41....

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Fructose, unlike glucose, does not stimulate insulin secretion from pancreatic  ß cells ( 40 41 ). The lack of stimulation by fructose is likely due to the low  concentrations of the fructose transporter GLUT5 in ß cells  ( 42 ).  Insulin is  involved in the regulation of body adiposity via its actions in the central  nervous system (CNS) to inhibit food intake and increase energy expenditure  ( see  reviews in references  43  and  44 ). Briefly, insulin receptors are localized in CNS  areas involved in the control of food intake and energy homeostasis. Insulin  administration into the CNS inhibits food intake in animals, including nonhuman  primates. Insulin does not enter the brain, but is transported into the CNS via a  saturable receptor-mediated process. Using compartmental modeling, Kaiyala et al  ( 45 ) showed that the obesity induced by a high-fat diet was associated with a 60%  reduction of the transport of insulin into the CNS in dogs. This impairment of central  insulin transport was inversely related to an increase in body weight in response to  high-fat feeding. Specifically, knocking out the insulin receptor in neurons results in  hyperphagia and obesity in mice ( 46 ). Thus, reduced insulin delivery into the CNS or  disruption of the insulin-signaling pathways in the CNS may result in weight gain and  the development of obesity. (  In 1980, Beck-Nielsen et al ( 94 ) investigated whether the reduction in insulin sensitivity induced by  sucrose consumption is related to the glucose or fructose components of the diet. They found that 7 d  of high-glucose feeding induced no significant changes in insulin sensitivity, whereas high-fructose  feeding was accompanied by both reductions in insulin binding and insulin sensitivity. Other  investigators found that diets containing 15% of energy as fructose produced undesirable changes in  glucose metabolism in both normal and hyperinsulinemic men ( 95 ). The classic relation between insulin resistance, increased fasting plasma insulin concentrations, and  glucose intolerance has been hypothesized to be mediated by changes in ambient nonesterified fatty  acid concentrations ( see  review in reference  96 ). Elevated nonesterified fatty acid concentrations are  one of the metabolic consequences of a chronic positive energy balance and increased body  adiposity ( 97 ). If, as discussed above,  fructose consumption leads to increased body weight as a  result of decreased insulin secretion and reduced leptin production, an increase in circulating  nonesterified fatty acids might follow . The exposure to increased concentrations of nonesterified 
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