Sensitivity to satiating and taste qualities of glucose in obese zucker rats

A general “glucoreceptor” defect, demonstrable in pancreatic islet and taste cells, may contribute to the metabolic and taste abnormalities of adult onset diabetes and possibly, if present at the level of the hypothalamus, could produce hyperphagia and the obesity seen in diabetics. To determine if a glucoreceptor defect generally accompanies obesity and glucose intolerance, behavioral responsiveness to glucose was examined in nine obese and nine lean female Zucker rats. Daily food and fluid intake were measured during three two-bottle preference tests, in which rats chose between water and one of several glucose solutions (1%, 3%, and 12%). Taste responsiveness to glucose of obese rats appeared normal; however, increased satiating effects of glucose were found in obese rats, possibly due to an enhanced delivery of glucose to neurons that inhibit feeding, caused by glucose intolerance. Also, obese rats had (a) increased brain weights, and (b) increased volumes of ventromedial and paraventricular hypothalamic nuclei. These findings, perhaps explainable by an increased delivery of nutrients to the developing brain, indicate that the hyperphagia of Zucker rats is due neither to an overt hypothalamic lesion nor to insensitivity to glucose.