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By G.D. Aurbach (Eds.)

ISBN-10: 0080866395

ISBN-13: 9780080866390

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Acceptance of these findings rests on the assumption that treatment with guanethidine has completely removed sympathetic innervation. , 1981; Levin and Sullivan, 1984). 3. Efferent Hormonal System A variety of endocrine systems are disturbed by VMH lesions. These include the release of growth hormone, the secretion of insulin, and the control of the reproductive cycle. In addition, the presence of adrenal corticosterone appears to be essential for the expression of obesity following both VMN and PVN lesions.

BRAY et al. while the final pathway(s1 responsible for generating the energy imbalance and the obesity may have many similarities between the various species, the precise genetic biochemical defects, located on a range of different chromosomes (Bray and York, 1979), may be varied and multiple. Interpretation of experimental data on the genetically obese models must also be viewed with qualification because, in the great majority of the studies, heterozygotes, which do not phenotypically express the obesity, are used as control animals.

1981). , 1980). Three main possibilities have been considered to explain the hypersecretion of insulin: altered control by the autonomic nervous system or by circulating factors, or defects within the pancreas and enteroinsular axis (see Section III,C,21. The levels of serum glucagon in the genetic obesities have not been so clearly defined as in the case of insulin. Numerous conflicting reports have suggested normal, enhanced, or decreased glucagon secretion in oblob, dbldb, and falfa mutants (see Bray and York, 19791, but all show an increase in the insulin-glucagon ratio.

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Advances in Research and Applications by G.D. Aurbach (Eds.)


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