Plasma gamma-glutamyltransferase is strongly determined by acylation stimulating protein levels independent of insulin resistance in patients with acute coronary syndrome

Jumana Saleh, Hatem Farhan, Ibtisam Al-Saqri, Bashair Al-Riyami, Katherine Cianflone

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background. Steatosis is a manifestation of the metabolic syndrome often associated with release of liver enzymes and inflammatory adipocytokines linked to cardiovascular risk. Gamma-glutamyltransferase (GGT) is one sensitive liver marker recently identified as an independent cardiovascular risk factor. Mechanisms involved in enhanced hepatic lipogenesis causing steatosis are not yet identified and are usually linked to insulin resistance (IR). Acylation stimulating protein (ASP), a potent lipogenic factor, was recently shown to increase in patients with steatosis and was implicated in its pathogenesis. Aim. To investigate the association of plasma ASP levels with liver and metabolic risk markers in acute coronary syndrome (ACS) patients. Methods. 28 patients and 30 healthy controls were recruited. Their anthropometrics, lipid profile, liver markers, insulin, and ASP levels were measured. Results. In the patients, ASP, liver, and metabolic risk markers were markedly higher than in the controls. ASP strongly predicted GGT levels (B = 0.75, P <0.0001), followed by triglycerides (B = 0.403, P = 0.017), together determining 57.6% variation in GGT levels. Insulin and IR correlated with metabolic risk components but not with liver enzymes. Conclusion. The strong association of ASP with GGT in ACS patients suggests that ASP, independent of IR, may contribute to a vicious cycle of hepatic lipogenic stimulation and GGT release promoting atherogenesis.

Original languageEnglish
Pages (from-to)155-161
Number of pages7
JournalDisease Markers
Volume35
Issue number3
DOIs
Publication statusPublished - 2013

ASJC Scopus subject areas

  • Biochemistry, medical
  • Clinical Biochemistry
  • Molecular Biology
  • Genetics

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