Effect of diet-induced obesity on glucose and insulin tolerance of a rodent with a low insulin response (Acomys cahirinus).
Gutzeit Arndt | Renold Albert E. | Cerasi Erol | Shafrir Eleazar
The role of environmental factors in the development of glucose intolerance was investigated by diet exchanges in spiny mice specimens from Geneva colonies (that tend to develop diabetes) and Jerusalem colonies (that do not). Jerusalem colony mice fed the Geneva diet (laboratory chow supplemented with high fat seeds) developed massive obesity and body lipid content increased compared to albino mice, spiny mice maintained in Jerusalem and spiny mice living in their natural habitat near the Dead Sea. Geneva colony mice maintained on laboratory chow alone were as lean as Jerusalem colony animals. The data suggest that in spiny mice, as in low insulin-responding humans, low insulin-secretory capacity is a major factor predisposing to glucose intolerance or to diabetes. When the insulin requirement is increased as a result of reduction of sensitivity to the hormone, the islets may not be able to adapt by a major increase in hormone secretion, and glucose intolerance may result. In this sense, obesity may be regarded as an additive factor in the development of diabetes.
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