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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 are unknown. In the present study, basal fat metabolism was characterized using a high-fat diet (HFD)-induced model of obesity development. Male rats consumed 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 body weight gain into obesity-prone (OP, > or =48 g) or obesity-resistant (OR, </=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 fat pads) at HFD1 was 26% greater and at HFD5 was 43% greater (P</=0.05) in OP vs. OR. Free fatty acid rates of appearance (FFA R(a)) and oxidation were not significantly different between OP and OR at 1 or 5 wk. Glycerol R(a), when expressed in absolute terms (micromol/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 as (3 x glycerol R(a)) - FFA R(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 expressed relative to fat cell volume (micromol. pl(-1). min(-1)), neither lipolysis nor intracellular cycling was significantly different between OP and OR, regardless of time on HFD. These data suggest that 1) if low rates of fat oxidation contribute to obesity development in OP rats, the contribution does not 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 lipolysis and reesterification may work to expand fat cell volume and increase fat pad weight in both OP and OR rats, although more so in OP rats.
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PMID:Fat oxidation, lipolysis, and free fatty acid cycling in obesity-prone and obesity-resistant rats. 1100 71

Obesity results from positive energy balance and, perhaps, abnormalities in lipid and glycogen metabolism. The purpose of this study was to determine whether differences in lipogenesis, retention of dietary fat, and/or glycogenesis influenced susceptibility to dietary obesity. After 1 wk of free access to a high-fat diet (HFD; 45% fat by energy) rats were separated on the basis of 1 wk body weight gain into obesity-prone (OP; > or =48 g) or obesity-resistant groups (OR; < or =40 g). Rats were either studied at this time (OR1, OP1) or continued on the HFD for an additional 4 wk (OR5, OP5). Weight gain and energy intake were greater (P < or = 0.05) in OP vs. OR at both 1 (53 +/- 2 vs. 34 +/- 1 g; 892 +/- 27 vs. 755 +/- 14 kcal) and 5 (208 +/- 7 vs. 170 +/- 7 g; 4,484 +/- 82 vs. 4,008 +/- 72 kcal) wk, respectively. Rats were injected with (3)H(2)O and were either provided free access to an HFD meal containing labeled fatty acids (fed; n = 10 or 11/group) or were fasted (n = 10/group) overnight. The amount of food or (14)C tracer eaten overnight was equivalent between OP and OR rats. In liver, the fraction of (3)H retained in glycogen or lipid was not significantly different between OR and OP groups. Retention of dietary fat in the liver was not increased in OP rats. In adipose tissue, retention of (3)H was approximately 49% greater (P < or = 0.05) in OP1 vs. OR1 and approximately 30% greater in OP5 vs. OR5, but retention of dietary fat was not elevated in OP vs. OR. At the same time, fat pad weight (sum of epididymal, retroperitoneal, mesenteric) was 49% greater in OP1 rats vs. OR1 rats and 65% greater in OP5 vs. OR5 rats (P < or = 0.05). Thus a greater capacity for lipogenesis or retention of dietary fat does not appear to be included in the OP phenotype. The characteristic increase in energy intake associated with OP rats appears to be necessary and critical to accelerated weight and fat gain.
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PMID:Inherent capacity for lipogenesis or dietary fat retention is not increased in obesity-prone rats. 1135 71