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IN attempting to evolve a unitary concept to explain the metabolic and clinical aberrations of diabetes mellitus, one is hard put to find a single defect that will satisfy all the known facts. Although there is widespread support for the pancreatic beta cell as the site of the defect of this disease, a scan of the literature indicates an impressive counterattack by those nominating the liver for this dubious honor.An analogous situation applies to our understanding of what is probably the most prevalent metabolic disorder of the age — simple obesity. After the development of immunoassay methods for measuring . . .
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Thomas J. Merimee (1971) studied this question.
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