Fat oxidation, lipolysis, and free fatty acid cycling in obesity-prone andobesity-resistant rats

Citation
Sr. Commerford et al., Fat oxidation, lipolysis, and free fatty acid cycling in obesity-prone andobesity-resistant rats, AM J P-ENDO, 279(4), 2000, pp. E875-E885
Citations number
31
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
ISSN journal
01931849 → ACNP
Volume
279
Issue
4
Year of publication
2000
Pages
E875 - E885
Database
ISI
SICI code
0193-1849(200010)279:4<E875:FOLAFF>2.0.ZU;2-C
Abstract
Defects in fat metabolism may contribute to the development of obesity, but what these defects are and where they occur in the feeding/fasting cycle a re unknown. In the present study, basal fat metabolism was characterized us ing a high-fat diet (HFD) induced model of obesity development. Male rats c onsumed a HFD (45% fat, 35% carbohydrate) ad libitum for either 1 or 5 wk ( HFD1 or HFD5). After 1 wk on the HFD, rats were separated on the basis of b ody weight gain into obesity-prone (OP, greater than or equal to 48 g) or o besity-resistant (OR, less than or equal to 40 g) groups. Twenty-four-hour- fasted rats were studied either at this time (OP1, OR1) or after 5 wk (OP5, OR5). Fat pad weight (sum of epididymal, retroperitoneal, and mesenteric f at pads) at HFD1 was 26% greater and at HFD5 was 43% greater (P less than o r equal to 0.05) in OP vs. OR. Free fatty acid rates of appearance (FFA Ra) and oxidation were not significantly different between OP and OR at 1 or 5 wk. Glycerol Ra, when expressed in absolute terms (mu mmol/min), increased from 1 to 5 wk of HFD feeding in both OP and OR, but significantly so only in OP. Likewise, increased rates of intracellular FFA cycling [estimated a s (3 x glycerol R-a) - FFAR(a)] were observed in both OP and OR rats from 1 to 5 wk of HFD feeding, but significantly so in OP rats only. When express ed relative to fat cell volume (mu mol.pl(-1).min(-1)), neither lipolysis n or intracellular cycling was significantly different between OP and OR, reg ardless of time on HFD. These data suggest that 1) if low rates of fat oxid ation contribute to obesity development in OP rats, the contribution does n ot occur at times when fat oxidation is at or near maximum rates (i.e., 24- h fasted conditions), and 2) between 1 and 5 wk of HFD feeding, basal lipol ysis and reesterification may work to expand fat cell volume and increase f at pad weight in both OP and OR rats, although more so in OP rats.