Potential role of vitamin d deficiency in nonalcoholic steatosis

K. Sudha, K. Reshma, Souparnika

Research output: Contribution to journalArticle

Abstract

Hypovitaminosis D is a wide spread and largely under recognizedpresent day epidemic. Since vitamin D undergoes activation in the liver, hepatic steatosis thought to be caused primarily due to insulin resistance can play a role in vitamin D deficiency. Hence the present study was conducted in 75 adult non diabetic patients in the age group of 25-55(45 males, 30 females) with hepatic steatosis. Liver function tests were estimated in the plasmaspectrophotometrically. Vitamin D was determined by ECLIA. Study groups included vitamin D deficient (group I), insufficient (group II) and sufficient groups (group III). Plasma ALT , ALP and total bilirubin levels were significantly higher in group I and II compared to group III patients. However, AST/ALT ratio was significantly higher groupIII compared to others. Plasma bilirubin and ALT showed significant negative correlation with vitamin D (r=-0.553,p=0.01) and AST/ALT ratio showed a positive correlation. The inverse association of vitamin D and hepatic markers attributes a possible hepatoprotective role of vitamin D. Patients with risk of impaired liver function need to be screened for vitamin D deficiency and its supplementation may prove beneficial.

Original languageEnglish
Pages (from-to)B133-B137
JournalInternational Journal of Pharma and Bio Sciences
Volume6
Issue number4
Publication statusPublished - 01-01-2015

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Avitaminosis
Vitamin D
Vitamins
Vitamin D Deficiency
Liver
Bilirubin
Liver Function Tests
Fatty Liver
Plasmas
Insulin Resistance
Age Groups
Chemical activation
Association reactions
Insulin

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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Potential role of vitamin d deficiency in nonalcoholic steatosis. / Sudha, K.; Reshma, K.; Souparnika.

In: International Journal of Pharma and Bio Sciences, Vol. 6, No. 4, 01.01.2015, p. B133-B137.

Research output: Contribution to journalArticle

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