Food Lipids: Chemistry, Nutrition, and Biotechnology

It has been suggested that n-3 polyunsaturated fatty acids may afford a protective
effect against diet-induced insulin resistance (215,237,243). Replacement of a
small portion (6–11%) of the fatty acids in a high-safflower oil diet with long chain
chain n-3 fatty acids from fish oil prevents the accumulation of intramuscular triglyceride
and development of insulin resistance typically observed in association
with consumption of a very high (59% calories) safflower oil diet (244,245). In
insulin-resistant slightly diabetic rats, 6 weeks of fish oil feeding corrected the inhibitory
effects of high-sucrose/high-fat feeding on insulin action (248). In that study,
adipocytes from the fish oil–fed rats, as compared with those of corn oil–fed rats,
had significantly higher rates of insulin-stimulated glucose transport, oxidation, and
incorporation into total lipids that were positively correlated with the fatty acid unsaturation
index of adipocyte membrane phospholipids. More recently, Podolin et al.
(243) reported that the insulin resistance typically induced in rats by high-sucrose
feeding could be prevented by adding as little as 6% fish oil to the diet. Recent data
from human studies indicate that the degree of insulin resistance is negatively correlated
to the amount of 22:6n-3 within skeletal muscle phospholipids (249). However,
long-term and beneficial effects of n-3 fatty acids on insulin action are not
consistently observed. Ezaki et al. (250) reported a stepwise increase in both insulinstimulated
glucose uptake and glucose transporter distribution following short-term
substitution (1-week) of a portion of the safflower oil in a high-fat diet with fish oil.
However, this effect is transient as further fish oil feeding (4 weeks) results in levels
of insulin resistance and adipose cell enlargement comparable to those observed with
the high-safflower diet. In addition, some human studies suggest that fish oil ingestion
may exacerbate existing type 2 diabetes (251).
3. Reversibility of Diet-Induced Alterations in Insulin Action
Prolonged consumption of a high-fat diet impairs insulin action and leads to the
development of obesity. Conversely, a reduction in dietary fat content may improve
insulin sensitivity and reduce obesity development. Harris and Kor (217) observed
an impaired insulin response to a glucose challenge in rats fed high-fat (40% energy)
diets for 8 weeks. This effect is reversed within 3 days following a modest reduction
in dietary fat content (30% energy). As alterations in body weight or fat content are
not observed until 14 days following the switch to the lower fat diet, the improvement
in insulin sensitivity is not believed to be secondary to a reduction in obesity (217).
Though the above results are encouraging, an improvement in insulin response upon
reduction in dietary fat content has not been consistently observed. In rats previously
fed high-fat (60% energy) diets for 6 months, Yakubu et al. (218) failed to detect
either an improvement in insulin response or a reduction in body weight following
subsequent consumption of a low-fat (20% energy) diet for 3 or 6 months. Thus,
alterations in insulin response induced by a high-fat diet and the reversibility of these
effects appear to be influenced by both level and type of dietary fat as well as the
duration of the high-fat feeding.
V. DIETARY FAT AND ADIPOSE TISSUE CELLULARITY
The expansion of adipose tissue during growth or the development of obesity is
achieved through an increase in adipose tissue size (cellular hypertrophy), an increase
in adipose tissue number (cellular hyperplasia), or through a combination of both
Copyright 2002 by Marcel Dekker, Inc. All Rights Reserved.