632 VI. OCCURRENCE OF LIPIDS IN THE ANIMAL 



of nutrient selection, a low overall oxygen consumption, low activity, and 

 an impaired resistance to cold. The rate of oxidation of injected radio- 

 acetate was likewise found to be depressed, as indicated by an increased 

 accumulation of fatty acids and cholesterol. The hyperglycemia is ex- 

 tremely resistant to insulin and is sensitive to diet and growth hormone. 

 In a later report, Mayer and co-workers 544 suggest that a main feature of 

 hereditary obesity in mice is their failure to oxidize C 2 fragments, with the 

 result that the pyruvate derived from carbohydrate is converted to fat 

 instead of being oxidized. It is postulated that a blocking of the hexoki- 

 nase reaction obtains under these conditions. 



These workers 543 are of the opinion that this hereditary obesity results 

 from an oversecretion of an alpha cell hormone of the islets of Langerhans. 

 When the alpha cells are destroyed by diethyl dithiocarbamate, the metab- 

 olism of such mice is completely changed. Thus, some weight loss takes 

 place, hyperglycemia disappears, blood glucose is no longer increased by the 

 administration of growth hormone, the oxidation of acetate becomes nor- 

 mal, and insulin resistance is greatly decreased. Mayer and Hagman 545 

 note that only 12% of the excess weight of obese animals is water; the 

 total proportion of the weight represented by water is similar in young obese 

 and non-obese animals of the same weight. 



Mayer 546 points out that obesity has a multiple etiology. According to 

 the glycostatic mechanism of regulation of food intake, appetite is regulated 

 by the rate of passage of glucose-phosphate into centers situated in the lat- 

 eral parts of the anterior hypothalamus ("feeding centers"). More central 

 centers, or "obesity" centers, act in part indirectly through the control of 

 the autonomic nervous system on the rate of lipogenesis and energy metabo- 

 lism. It is suggested that hyperphagia results from the activation of the 

 lateral centers, inactivation of the central centers, lesions of the frontal or 

 thalamic association fibers or frontal centers, hypoglycemia, a block of the 

 hexokinase reaction or, indirectly, from an increased lipogenesis, metabolic 

 inertia of depot fat, or from abnormalities in metabolism resulting from im- 

 mobilization. In the case of the hereditary obese-hyperglycemic syn- 

 drome, the role of the endocrine glands also appears to be fundamental in 

 the etiology of the obesity. Hypersecretion of a pancreatic hormone other 

 than insulin is believed to be primarily responsible for this condition. 



644 J. Mayer, R. E. Russell, M. W. Bates, and M. M. Dickie, Metabolism, 2, 9-21 

 (1953). 



546 J. Mayer and N. C. Hagman, Proc. Soc. Exptl. Biol. Med., 82, 647-649 (1953). 



646 J. Mayer, Absl. XIX Intern. Physiol. Congr., Montreal (Aug.-Sept., 1953), pp. 

 598-599. 



