Food Lipids: Chemistry, Nutrition, and Biotechnology

Figure 2 Proposed mechanism for paracrine/autocrine regulation of adipose cell development.
the specific diet-induced alterations in adipose tissue cellularity may be a major factor
influencing the reversal of the obese state (258,278). Thus, obesity associated with
changes in fat cell size is readily reversed only when the animals are returned to a
low-fat regime (258,278). However, this is not the case for obesity associated with
changes in fat cell number. Diet-induced changes in fat cell number appear to be
permanent, as substitution of a high-fat diet with a low-fat diet leads to reductions
in body weight and fat cell size but not in fat cell number (258,278,279). Thus, a
permanent increase in the capacity for energy storage and in the potential for expansion
of adipose tissue mass would be a consequence of long-term exposure to
the high-fat feeding. As mentioned previously (Sec. II), high levels of dietary fat
have been associated with the development of obesity in humans. If the observations
regarding cellularity alterations and the potential reversal of obesity are indeed applicable
to humans, this would suggest that high-fat diet–induced obesity, particularly
that of extended duration, may be resistant to intervention and may also have
long-term metabolic consequences.
REFERENCES
1. E. N. Whitney and S. R. Rolfes. Energy balance and weight control. In: Understanding
Nutrition (E. N. Whitney and S. R. Rolfes, eds.). West Publishing Co., New York,
1993, p. 254.
2. National Research Council (NRC). Diet and Health: Implications for Reducing Chronic
Disease Risk. National Academy Press, Washington, DC, 1989, p. 563.
3. V. S. Hubbard. Prevention of obesity: Populations at risk, etiologic factors and intervention
strategies. Obes. Res. 3:76S (1995).
Copyright 2002 by Marcel Dekker, Inc. All Rights Reserved.