title: Measurement of liver fat by MRI and its reduction by dexfenfluramine in NIDDM.
abstract: OBJECTIVE
  To validate a variation of a well-established magnetic resonance imaging (MRI) technique to detect liver fat and use it to monitor liver fat changes after treatment with dexfenfluramine in men with non-insulin dependent diabetes mellitus (NIDDM).
  
  
  METHODS
  (a) Simple correlation study of MRI Liver Fat Index with liver biopsy results; (b) Open Study of 10 men with NIDDM treated with dexfenfluramine for 12 weeks in addition to their 'usual' therapy.
  
  
  METHODS
  (a) 19 patients (3F; 16M) with abnormal liver function tests undergoing liver biopsy; (b) 10 men, Body Mass Index (BMI) < 30, Waist to hip ratio (WHR) > 0.90 with poorly controlled NIDDM despite oral sulphonylurea therapy.
  
  
  METHODS
  (a) MRI liver fat; standard liver biopsy; (b) MRI visceral fat, MRI liver fat, euglycaemic clamp, plasma lipids, fasting glucose and c-peptide levels.
  
  
  RESULTS
  In the validation group, there was a strong relationship between the MRI Liver Fat Index and histopathological assessment of the liver biopsies (r = 0.87, < 0.0001). During treatment with dexfenfluramine the mean Liver Fat Index reduced from 10.6 +/- 3.4 to 6.6 +/- 2.8 (P = 0.05). The reduction in Liver Fat Index correlated with the reduction in visceral fat (r = 0.84, P = 0.001) as well as with the improvement in insulin sensitivity (r = 0.62, P = 0.05). Using partial correlation analysis, the relationship between the change in visceral adipose tissue and the improvement in insulin sensitivity was weaker if the Liver Fat Index was kept constant (r = 0.76 decreased to r = 0.56).
  
  
  CONCLUSIONS
  In this group of subjects MRI Liver Fat Index correlated well with liver fat as seen on biopsy. The Liver Fat Index reduced after 12 weeks therapy with dexfenfluramine suggesting a role for hepatic steatosis in the complex interaction between visceral adipose tissue and insulin sensitivity.
authors.affiliation: Diabetes Unit, Radcliffe Infirmary, Oxford, Melbourne, Australia.
authors.forename: S J
authors.initials: SJ
authors.lastname: Marks
authors.forename: N R
authors.initials: NR
authors.lastname: Moore
authors.forename: N G
authors.initials: NG
authors.lastname: Ryley
authors.forename: M L
authors.initials: ML
authors.lastname: Clark
authors.forename: J J
authors.initials: JJ
authors.lastname: Pointon
authors.forename: B J
authors.initials: BJ
authors.lastname: Strauss
authors.forename: T D
authors.initials: TD
authors.lastname: Hockaday
mesh_terms: D000328:Adult; D001706:Biopsy; D016001:Confidence Intervals; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000473:pathology*; D005234:Fatty Liver / Q000188:drug therapy* / Q000473:pathology*; D005260:Female; D005277:Fenfluramine / Q000627:therapeutic use*; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009765:Obesity; D017367:Selective Serotonin Reuptake Inhibitors / Q000627:therapeutic use*
chemical_list: D005277:Fenfluramine; D017367:Selective Serotonin Reuptake Inhibitors