Dietary fat, genetic predisposition, and obesity: lessons from animal models

Abstract

This review focuses on animal studies that examine the role of dietary fat in obesity. It is evident from animal experiments that the percentage of energy derived from fat in the diet is positively correlated with body fat content. With few exceptions, obesity is induced by high-fat diets in monkeys, dogs, pigs, hamsters, squirrels, rats, and mice. The mechanisms responsible for this correlation between body fat and dietary fat content are not clear. It has been proposed that a high-fat diet produces hyperphagia, which is solely responsible for the increased body fat content. However, several studies in various rodent models showed that increased body fat content still results when the hyperphagia is prevented. This suggests that some metabolic effects of high-fat diets, independent of hyperphagia, may also be contributing to the obesity induced by high-fat diets. It is also clear from animal studies that genetic factors significantly modulate the body's response to diets high in fat-derived energy. In contrast with the animal studies, studies in humans that have examined the relation between dietary fat content and body fat are inconclusive. The limitations of cross-sectional studies, the lack of controlled feeding trials, and the importance of genetic variation in response explain the absence of conclusive evidence. The lessons learned from animal models point to dietary fat as one potentially important component in the etiology of human obesity. Additional comprehensive studies are warranted to determine the role of dietary fat in the etiology of human obesity.

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

“…The high palatability of fatty diets often leads to hyperphagia and thus weight gain, but not always. 58 Weight gain can occur in spite of decreased food consumption when on a high-fat diet, perhaps due to differences in the efficiency of storage or thermic effects of digestion. 19,32,58,59 The WD used in this study has very high levels of saturated fats and added sucrose, both of which are considered unhealthy if ingested frequently because they can contribute to the metabolic syndrome and other chronic diseases.…”

Dietary fat and fat types as early determinants of childhood obesity: a reappraisal

“…Nevertheless, several studies have demonstrated that body fat can increase on a high-fat diet when an increase in energy intake is prevented. 33,34 Pre-and post-natal recommendations for PUFA and LC-PUFA The EFA, that is, linoleic acid (LA, 18:2n-6) and a-linolenic acid (ALA, 18:3n-3), belong to the family of polyunsaturated fatty acids (PUFA). LA and ALA serve as essential precursors for producing their respective long-chain products (LC-PUFA), arachidonic acid (ARA, 20:4n-6) and both eicosapentaenoic acid (EPA.…”

Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet

“…1 One of the major public health concerns in this century is the medical consequences stemming from the ready availability of high-fat, energy-dense foods, as this is one of the fundamental causes of the obesity epidemic. 2 Physiological experiments illustrate that energy-dense diets can potentially compromise normal appetite regulation in humans. 3 This study aimed to specifically explore the impact of palatable foods on appetite and metabolic regulation.…”