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Equine veterinary journal1992; 24(5); 341-346; doi: 10.1111/j.2042-3306.1992.tb02852.x

Plasma lipids, lipoproteins and post-heparin lipases in ponies with hyperlipaemia.

Abstract: The metabolic origins of equine hyperlipaemia were investigated by analysing the concentration and composition of plasma lipoproteins in 18 ponies with the condition. The mean concentrations of cholesterol, triglyceride and very low density lipoproteins (VLDL) were increased by 4-, 52- and 19-fold, respectively, compared with a control group of 18 healthy ponies. These increases were due to the appearance of a buoyant VLDL fraction (VLDL1) not present in healthy ponies. The mean diameter of VLDL1 particles was 44% greater than control VLDL, and the particles were enriched in triglyceride and free cholesterol and depleted of cholesteryl esters, phospholipid and protein. The apolipoprotein (apo) B-100 content of VLDL1 was reduced and the ratio of apoB-100 to apoB-48 particles was 1:1, compared with 2:1 in control VLDL. The VLDL1 was also enriched in apoE, but had normal complements of apoC-II and apoC-III. The conventional VLDL (called VLDL2), LDL and HDL fractions were moderately enriched with triglyceride, and HDL contained increased amounts of apoE, apoC-II and apoC-III. The activities of lipoprotein lipase and hepatic lipase, the enzymes responsible for the catabolism of VLDL and their remnants, were increased by 2- and 3-fold, respectively, in response to the increased concentrations of their substrates. The composition of VLDL1 suggested that the liver was maximising the secretion of triglyceride by producing larger number of VLDL particles that accommodated a greater mass of triglyceride by having apoB-48 rather than apoB-100 as their structural protein. Plasma free fatty acid (FFA) concentrations were elevated in 17 of the 18 ponies, suggesting that increased FFA flux might be the stimulus for hepatic triglyceride synthesis and VLDL secretion. We conclude that overproduction, rather than defective catabolism, of VLDL was the cause of the hyperlipidaemia and that lipid lowering agents which reduce VLDL synthesis, by decreasing adipose lipolysis and FFA flux, are candidates for the management of hyperlipaemia.
Publication Date: 1992-09-01 PubMed ID: 1396507DOI: 10.1111/j.2042-3306.1992.tb02852.xGoogle Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research investigates the metabolic origins of equine hyperlipaemia by analysing plasma lipoproteins in ponies affected by this condition, and suggests that overproduction of VLDL, not faulty catabolism, is the cause.

Objective and Methodology of the Research

  • The research aimed to understand the origins of equine hyperlipaemia, a disorder where there is an excessive amount of lipids (fats) in the blood, by investigating the concentration and makeup of plasma lipoproteins in ponies with this condition.
  • A total of 18 ponies with hyperlipaemia were analysed and compared against a control group of 18 healthy ponies.
  • The metabolic components, including cholesterol, triglyceride, and very low-density lipoproteins (VLDL) levels, were measured and compared.

Findings

  • A significant increase in mean concentrations of cholesterol, triglyceride, and VLDL levels were found in the ponies with hyperlipaemia.
  • Among the observations, a new lipoprotein fraction, named VLDL1, was discovered to be prevalent in ponies with hyperlipaemia but absent in healthy ponies. This VLDL1 was found to be enriched in triglyceride and free cholesterol, but deficient in cholesteryl esters, phospholipid, and protein.
  • The ratio of apoB-100 to apoB-48 particles was also different in VLDL1 than the normal ratio present in control VLDL, with more apoE present in the VLDL1.
  • Despite the overproduction of VLDL particles, the liver had increased activities of lipoprotein lipase and hepatic lipase, the enzymes responsible for breaking down VLDL and its remnants, suggesting that the liver was trying to cope with the increased concentration of substrate.

Conclusion

  • The findings led researchers to conclude that it was the overproduction of VLDL, not the faulty catabolism, causing the hyperlipaemia. This meant that it wasn’t that the body was unable to break down the lipids but that more VLDL than normal was being produced in the first place.
  • The 17 out of 18 ponies with hyperlipaemia showed increased plasma free fatty acid (FFA) concentrations, leading the team to suggest that an increased FFA flux could be stimulating the liver to synthesise more triglyceride and secrete more VLDL.
  • The researchers propose lipid-lowering agents as potential treatment options for managing hyperlipaemia in ponies. The agents would work by reducing VLDL synthesis, thus decreasing adipose lipolysis and FFA flux.

Cite This Article

APA
Watson TD, Burns L, Love S, Packard CJ, Shepherd J. (1992). Plasma lipids, lipoproteins and post-heparin lipases in ponies with hyperlipaemia. Equine Vet J, 24(5), 341-346. https://doi.org/10.1111/j.2042-3306.1992.tb02852.x

Publication

ISSN: 0425-1644
NlmUniqueID: 0173320
Country: United States
Language: English
Volume: 24
Issue: 5
Pages: 341-346

Researcher Affiliations

Watson, T D
  • Department of Pathological Biochemistry, Royal Infirmary, Glasgow, UK.
Burns, L
    Love, S
      Packard, C J
        Shepherd, J

          MeSH Terms

          • Animals
          • Cholesterol / blood
          • Cholesterol, VLDL / blood
          • Heparin
          • Horse Diseases / blood
          • Horses
          • Hyperlipidemias / blood
          • Hyperlipidemias / veterinary
          • Lipase / blood
          • Lipids / blood
          • Lipoprotein Lipase / blood
          • Lipoproteins / blood
          • Lipoproteins, VLDL / blood
          • Liver / enzymology

          Citations

          This article has been cited 3 times.
          1. Kosinska MK, Eichner G, Schmitz G, Liebisch G, Steinmeyer J. A comparative study on the lipidome of normal knee synovial fluid from humans and horses.. PLoS One 2021;16(4):e0250146.
            doi: 10.1371/journal.pone.0250146pubmed: 33861772google scholar: lookup
          2. Adolph S, Schedlbauer C, Blaue D, Schöniger A, Gittel C, Brehm W, Fuhrmann H, Vervuert I. Lipid classes in adipose tissues and liver differ between Shetland ponies and Warmblood horses.. PLoS One 2019;14(3):e0207568.
            doi: 10.1371/journal.pone.0207568pubmed: 30897169google scholar: lookup
          3. Ranjithkumar M, Malik TA, Saxena A, Dan A, Sakthivel PC, Dey S. Hyperlipidaemia in trypanosomiasis of naturally infected horses: possible cachexia-anorexia syndrome?. Trop Anim Health Prod 2013 Feb;45(2):417-21.
            doi: 10.1007/s11250-012-0232-zpubmed: 22836485google scholar: lookup