A low α-linolenic intake during early life increases adiposity in the adult guinea pig

Abstract

BackgroundThe composition of dietary fatty acids (FA) during early life may impact adult adipose tissue (AT) development. We investigated the effects of α-linolenic acid (ALA) intake during the suckling/weaning period on AT development and metabolic markers in the guinea pig (GP).MethodsNewborn GP were fed a 27%-fat diet (w/w %) with high (10%-ALA group), moderate (2.4%-ALA group) or low (0.8%-ALA group) ALA content (w/w % as total FA) until they were 21 days old (d21). Then all animals were switched to a 15%-fat diet containing 2% ALA (as total FA) until 136 days of age (d136).ResultsALA and docosapentaenoic acid measured in plasma triglycerides (TG) at d21 decreased with decreasing ALA intake. Total body fat mass was not different between groups at d21. Adipose tissue TG synthesis rates and proliferation rate of total adipose cells, as assessed by 2H2O labelling, were unchanged between groups at d21, while hepatic de novo lipogenesis was significantly 2-fold increased in the 0.8%-ALA group. In older GP, the 0.8%-ALA group showed a significant 15-%-increased total fat mass (d79 and d107, p < 0.01) and epididymal AT weight (d136) and tended to show higher insulinemia compared to the 10%-ALA group. In addition, proliferation rate of cells in the subcutaneous AT was higher in the 0.8%-ALA (15.2 ± 1.3% new cells/5d) than in the 10%-ALA group (8.6 ± 1.7% new cells/5d, p = 0.021) at d136. AT eicosanoid profiles were not associated with the increase of AT cell proliferation.ConclusionA low ALA intake during early postnatal life promotes an increased adiposity in the adult GP.

Linoleic acid and the pathogenesis of obesity

“…A study investigating the impact of differing ALA contents in neonatal guinea pigs using LA to primarily offset energy contribution of ALA found that 3 weeks of low ALA feeding (0.8 % total fat) (high LA feeding) followed by a chow diet for 16 weeks resulted in a 15% increase in fat mass at 19 weeks of age. In addition these animals had higher adipose tissue proliferation rates than those fed an isoenergetic (with matched fat content) 10% ALA diet [111]. Though the animals in this study were not fed by their mothers, it is possible to infer the effect of feeding a low ALA/high LA diet in the early postnatal period on subsequent body composition and adipocyte proliferation.…”

Early Low-Fat Diet Enriched With Linolenic Acid Reduces Liver Endocannabinoid Tone and Improves Late Glycemic Control After a High-Fat Diet Challenge in Mice

“…Recent studies (24) have shown that perinatal exposure to a rich n-6 FA diet is able to induce obesity and to affect body fat mass across generations. On the other hand, the beneficial role of dietary n-3 FA during early life has been emphasized because n-3 FA deficiency increases adiposity in guinea pigs (25). This idea was reinforced by the study of Massiera et al (26), showing that the addition of a-linolenic acid (a-LNA [or C18:3n-3]) to an LA-rich high-fat diet (HFD) under isolipidic and isocaloric conditions reduces the deleterious Figure 1-Schematic illustration of the pathways for biosynthesis and degradation of ECs (A) and the experimental study design (B).…”

Synergism of α‐Linolenic Acid, Conjugated Linoleic Acid and Calcium in Decreasing Adipocyte and Increasing Osteoblast Cell Growth

“…According to the recent review by Kim and Ilich (2011) [22], osteoporotic animals given ALA-rich diets showed improved bone properties, which was strengthened when combined with estrogen therapy or in various pathological conditions. Furthermore, in some animal studies ALA-rich diets resulted in a significant reduction in body weight, visceral adiposity and leptin [12,23], whereas ALA- deficient diets led to a significant increase in hepatic de novo lipogenesis, total/epididymal fat mass and adipocyte proliferation [24]. The increase of adipose tissue observed in obesity involves both hypertrophy of pre-existing adipocytes and hyperplasia by forming new adipocytes from precursor cells (adipogenesis) [25,26].…”