Contemporary Metabolism

1. Front Matter

   Pages i-xxiv

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2. Diabetes Mellitus Selected Aspects of Pathophysiology and Clinical Practice

   • Daniel Porte Jr., Jeffrey B. Halter, Christoph de Haën, Jerry P. Palmer, Christopher M. Asplin, Ronald J. Graf et al.

   Pages 1-59

3. Glucagon Secretion, Function, and Clinical Role

   • Richard E. Dobbs, Roger H. Unger

   Pages 61-118

4. Hypothalamic-Pituitary Function in Obesity

   • Bruce S. Schneider, Jules Hirsch

   Pages 119-144

5. Plasma Apolipoproteins and Lipoprotein Receptors

   • Howard A. Eder

   Pages 145-175

6. Alcohol, Amino Acids, and Encephalopathy

   • Spencer Shaw, Charles S. Lieber

   Pages 177-187

7. GABA and Taurine What Are Metabolites Like This Doing in Places Like That?

   • Rima Rozen, Paul R. Goodyer, Charles R. Scriver

   Pages 189-237

8. Nutrition and Aging

   • Myron Winick, Michael W. Hamm, S. Jaime Rozovski

   Pages 239-245

9. Receptors and Second Messengers in Cell Function and Clinical Disorders

   • E. M. Brown, G. D. Aurbach

   Pages 247-299

10. Stimulated Phosphatidylinositol Turnover A Brief Appraisal

    • R. F. Irvine, R. M. C. Dawson, N. Freinkel

    Pages 301-342

11. Disorders of Purine and Pyrimidine Metabolism Basic and Clinical Considerations

    • J. Edwin Seegmiller

    Pages 343-409

12. Metabolic Aspects of Urinary Stone Disease

    • Edwin L. Prien Jr., Hibbard E. Williams

    Pages 411-439

13. The Divalent Ions Calcium, Phosphorus, and Magnesium and Vitamin D

    • Nachman Brautbar, David B. N. Lee, Charles R. Kleeman

    Pages 441-526

14. Back Matter

    Pages 527-540

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It is abundantly clear that a number of subtle abnormalities in hypothalamic function are associated with human obesity. Some hormonal abnormalities-the diminished growth hormone responses, for example-are critically dependent on increased caloric intake and are quickly reversible with weight loss. Others, such as the blunted prolactin response to acute hypoglycemia, may persist in the reduced-obese state. Still others (e. g. , the blunted ACTH responses to insulin­ induced hypoglycemia) may, in some patients, first appear in the reduced-obese state. It remains uncertain whether any of these abnormalities is ever antecedent to the presence of obesity. Obviously, it is difficult to plan experiments in which the amounts of stored triglyceride, the level of caloric intake, and the state or his­ tory of obesity can all be individually evaluated. The issue is made even more complex by the fact that there may be subgroups of obese in whom hypothalamic function may be abnormal, whereas many obese may have nearly normal hypo­ thalamic function. It should be remembered that for years clinicians and investigators, working with available research tools, have ruled out pituitary or hypothalamic abnor­ malities as a cause of human obesity. These tools have oftentimes been no more sophisticated than skull roentgenograms and samples of excreted steroid hormones in 24-hr urine. The advent of radioimmunoassays for peptide hormones and the availability of synthetic releasing hormones have offered possibilities of studying hypothalamic function undreamed of just a few years ago.

• Calcium
• Colon
• DNA
• Glycogen
• Nucleotide
• Purine
• Pyrimidine
• alcohol
• chemistry
• enzyme
• enzymes
• kidney
• metabolism
• mutation
• proteins

• Northwestern University Medical School, Chicago, USA

  Norbert Freinkel

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