Abstract
were allowed to eat ad libitum or were fed 2 grams of food per day. The ad-libitum fed obese mice ate more than ad-libitum fed normal mice and had a shorter length of life. However, the calorie-restricted obese mice had a greater maximum longevity than ad-libitum fed normal mice even though the body fat con tent of the calorie-restricted obese mice was more than twice that of the ad-libitum fed normal mice. Barzilai and Gupta criti cize this study because visceral fat was not separately mea sured, a flaw shared by all of the early studies. Barzilai and Gupta also feel these obese mice are a poor model because they lack a functional leptin peptide. I disagree because caloric re striction increased the longevity of these obese mice, and that indicates a reduction in leptin is not involved in the antiaging action of caloric restrietion. In contrast to the view of Barzilai and Gupta, I believe that the available evidence makes a strong case against reduction in body fat playing a role in the antiaging action of caloric restric tion. However, I strongly feel that this issue can and should be reassessed by using modem technology that permits noninva sive, longitudinal measures of total and specific depot fat. If such a study indicates a role for reduction of body fat, then the many endocrine and metabolie mechanisms suggested in this hypothesis article would be worth pursuing.
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