Obesity and Diabetes

Noninsulin-dependent or adult-onset diabetes (NIDDM) affects nearly 10 million people in the United States, but obesity can be found in 10 times that number. Both diseases have high heritability but are also markedly influenced by the environment. Dietary and other life style changes appear to be responsible for a recent great increase in the expression of the obesity and diabetes genes. This close relationship between obesity and diabetes has been a cause for much investigation and speculation. One might consider obesity as a compensated form of NIDDM, which in some genetic backgrounds is decomposed to florid diabetes by the stress of environmental factors. Both obesity and diabetes show alterations in pancreatic function, carbohydrate intolerance, and hepatic overproduction of glucose. How the action of one or even several genes can produce these three alterations of physiology remains unknown and thus the basic nature of the obesity-diabetes remains a mystery. One guess is that hypothalamic controls mediated by the activity of the autonomic nervous system along with the effects of a variety of peptides, all of which normally act in concert to maintain a given level of fat storage and of blood glucose level, become disordered. Since this control system has many components, the disorders can arise at many different sites. Because of the interest of my laboratory in adipose tissue, I have elected, in this brief essay, to examine those changes in adipose tissue which may play a role in the obesity-diabetes link.