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© 2006 American Society for Nutrition J. Nutr. 136:2980-2986, December 2006


Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Adipose Fatty Acid Composition and Rate of Incorporation of {alpha}-Linolenic Acid Differ between Normal and Lipoprotein Lipase-Deficient Cats1,2

Brian C. Veltri3, Robert C. Backus5,*, Quinton R. Rogers4 and Edward J. DePeters3

3 Department of Animal Science and 4 Department of Molecular Biosciences, University of California, Davis, CA 95616 and 5 Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211

* To whom correspondence should be addressed. E-mail: backusr{at}missouri.edu.

Normal adiposity occurs in humans and mice deficient of adipose lipoprotein lipase (LPL) activity. Subnormal adiposity found in LPL-deficient cats is indicative of limited de novo synthesis of fatty acids (FAs). In 14 LPL-deficient (3.0 ± 0.1 kg) and 8 normal (3.7 ± 0.1 kg) queens, FAs in triacylglycerol (TAG), phospholipid (PL), and nonesterified FAs (NEFAs) of plasma and inguinal subcutaneous adipose were determined before and after (d 38, 61, 110, 117, and 251) dietary linseed oil supplementation (30 g/kg). By d 60, LPL-deficient queens gained body weight (+0.4 ± 0.1 kg), developed normal body fat mass (25 ± 2%), and were enriched in 18:3(n-3) in their plasma and adipose lipids. Adipose TAG 18:3(n-3) enrichment in LPL-deficient queens was subnormal at all sampling times and, as observed in normal queens, apparently not equilibrated by d 251. Adipose FA profiles in TAG but not PL were substantially different (P < 0.05) between LPL-deficient and normal queens; the 16:0 to 18:2(n-6) ratio was high in LPL-deficient (2.4–4.4) relative to normal queens (1.0–1.4). In LPL-deficient queens, fed-state plasma NEFA (n-6) and (n-3) enrichments were similar to those in adipose TAG, and plasma NEFA concentration was high (0.62 ± 0.05 mmol/L) and similar to that in normal queens after withholding diet for 16 h. These data indicate that LPL deficiency in cats reduces dietary FA storage efficiency, favors storage of saturated over unsaturated FAs, and stimulates de novo FA synthesis substantive enough to support normal adiposity.








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