Spiny mice (Acomys cahirinus) from the Geneva colony tend to develop diabetes, whereas those maintained in Jerusalem do not. The role of environmental factors in the development of glucose intolerance was investigated by diet exchanges in specimens from the two colonies. Spiny mice on the Geneva diet (laboratory chow supplemented by a seed mixture containing 15% fat by weight) developed massive obesity over 8–10 months; body lipid content increased threefold compared with albino mice and was twofold higher than in spiny mice maintained on the laboratory chow in Jerusalem or in spiny mice living in their natural habitat near the Dead Sea. Spiny mice from the Geneva colony, kept on the laboratory chow alone, were as lean as animals from the Jerusalem colony. Similarly, Jerusalem Acomys given pellets supplemented by seeds developed marked obesity. Liver and adipose tissue enzymes in spiny mice transferred to the seed-supplemented diet showed adaptation typical for fat feeding: decrease in the capacity of glycolysis, NADPH generation, and fatty acid synthesis.

The obesity was associated with insulin resistance, evident from a negative correlation between the extent of hypoglycemia after i.v. insulin administration and body lipid content. The glucose disappearance rate (K value) was significantly reduced by obesity, but the insulin response to i.v. glucose increased only moderately. In all the Acomys groups studied, insulin response to i.v. glucose was markedly lower in comparison with the response in albino mice.

The following conclusions are drawn: (1) Low insulin response to glucose is a species-characteristic of spiny mice whether the animals are bred in laboratories or live in freedom. (2) Given an appropriate diet, spiny mice develop obesity, accompanied by pronounced insulin resistance. (3) Obesity may be one of the causes of the marked islet hyperplasia in laboratory-kept spiny mice, but this does not result in increased insulin output. (4) The inability of spiny mice to respond with augmented insulin secretion when insulin efficiency is reduced may be responsible for the accelerated development of glucose intolerance in this species. Thus, the liability of Geneva spiny mice to develop diabetes may be caused by the obesity-inducing diet used in this colony rather than to a specific genetic characteristic. (5) The fact that insulin resistance in spiny mice occurs without the development of hyperinsulinemia suggests that similar mechanisms may operate in the development of glucose intolerance in human, low, insulin responders.

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