Highly reproducible values of ADC and FA were obtained with the polygonal method on intra-rater (coefficients of variation

OBJECTIVEWeight loss through lifestyle changes is recommended for nonalcoholic fatty liver disease (NAFLD). However, its efficacy in patients with type 2 diabetes is unproven.RESEARCH DESIGN AND METHODSLook AHEAD (Action for Health in Diabetes) is a 16-center clinical trial with 5,145 overweight or obese adults with type 2 diabetes, who were randomly assigned to an intensive lifestyle intervention (ILI) to induce a minimum weight loss of 7% or a control group who received diabetes support and education (DSE). In the Fatty Liver Ancillary Study, 96 participants completed proton magnetic resonance spectroscopy to quantify hepatic steatosis and tests to exclude other causes of liver disease at baseline and 12 months. We defined steatosis >5.5% as NAFLD.RESULTSParticipants were 49% women and 68% white. The mean age was 61 years, mean BMI was 35 kg/m2, mean steatosis was 8.0%, and mean aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were 20.5 and 24.2 units/l, respectively. After 12 months, participants assigned to ILI (n = 46) lost more weight (−8.5 vs. −0.05%; P < 0.01) than those assigned to DSE and had a greater decline in steatosis (−50.8 vs. −22.8%; P = 0.04) and in A1C (−0.7 vs. −0.2%; P = 0.04). There were no significant 12-month changes in AST or ALT levels. At 12 months, 26% of DSE participants and 3% (1 of 31) of ILI participants without NAFLD at baseline developed NAFLD (P < 0.05).CONCLUSIONSA 12-month intensive lifestyle intervention in patients with type 2 diabetes reduces steatosis and incident NAFLD.

KeywordsBrain tumors; magnetic resonance spectroscopy; spectroscopic imaging; metabolites IntroductionLocalized proton MR spectroscopy (MRS) of the human brain, first reported more than 20 years ago,(1-3) is a mature methodology that is used clinically in many medical centers worldwide for the evaluation of brain tumors.(4) While there have been studies of human brain tumors using heteronuclei such as phosphorus ( 31 P) and sodium ( 11 Na),(5,6) by far the most spectroscopy studies use the proton ( 1 H) nucleus, because of both its high sensitivity and ease of implementation on commercial MRI scanners. This review will therefore focus on proton MRS in human brain tumors.There are two classes of spatial localization techniques for MR spectroscopy; single-voxel (SV) techniques (commonly used methods includes 'PRESS'(7) and 'STEAM'(8)) which record spectra from one region of the brain at a time, or multi-voxel techniques ('MR spectroscopic imaging' (MRSI), also called 'Chemical Shift Imaging' (CSI)(9)) which simultaneously record spectra from multiple regions and thereby map out the spatial distribution of metabolites within the brain. MRSI is typically performed in 2-or 3-dimensions, but does not usually include full brain coverage. While SV-MRS and MRSI each have their own advantages and disadvantages (e.g. in terms of spectral quality, scan time, spatial resolution, spatial coverage, and ease of use/interpretation), a key consideration for brain tumors is their metabolic inhomogeneity. For instance, the spectrum from the necrotic core of a high-grade brain tumor is quite different from a spectrum from the actively growing rim, while peri-tumoral edema is different from tumor invasion into surrounding brain tissue; for these reasons and others, high-resolution MRSI is often favored for evaluating brain tumor metabolism. For a detailed discussion of the relative merits of SV-MRS and MRSI, please see reference. (10) © 2010 Elsevier Inc. All rights reserved. 2 Author for Correspondence: Professor, Russell H Morgan Department of Radiology and Radiological Science, Department of Radiology, Park 367B, Johns Hopkins University School of Medicine, 600 N Wolfe Street, Baltimore, MD 21287, Phone (410) 955-1740, FAX (410) pbarker2@jhmi.edu. 1 Phone (410) 614-2707, FAX (410) 502-6076, ahorska@jhmi.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroimaging Clin N Am. Author manuscript; available in PMC 2011 August 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptEarly in the development of human brain proto...

Fructose consumption predicts increased hepatic fibrosis in those with nonalcoholic fatty liver disease (NAFLD). Due to its ability to lower hepatic adenosine triphosphate (ATP) levels, habitual fructose consumption could result in more hepatic ATP depletion and impaired ATP recovery. The degree of ATP depletion following an intravenous fructose challenge test in low versus high fructose consumers was assessed. We evaluated diabetic adults enrolled in the Look AHEAD Fatty Liver Ancillary Study (n=244) for whom dietary fructose consumption estimated by a 130-item Food Frequency questionnaire, hepatic ATP measured by phosphorus MRS (31P MRS) and uric acid (UA) levels were performed (n=105). In a subset of participants (n=25), an intravenous fructose challenge was utilized to assess change in hepatic ATP content. The relationships between dietary fructose, UA and hepatic ATP depletion at baseline and following intravenous fructose challenge was evaluated in low (<15 g/d) vs. high (≥15 g/d) fructose consumers. High dietary fructose consumers had slightly lower baseline hepatic ATP levels and a greater absolute change in hepatic α-ATP/Pi ratio (0.08 vs. 0.03, p=0.05) and γ-ATP /Pi ratio following an intravenous fructose challenge (0.03 vs. 0.06, p=0.06). Patients with high UA (≥5.5 mg/dl) showed a lower minimum liver ATP/Pi ratio post-fructose challenge (4.5 vs. 7.0, p = 0.04). Conclusions High fructose consumption depletes hepatic ATP and impairs recovery from ATP depletion following an intravenous fructose challenge. Subjects with high UA show a greater nadir in hepatic ATP in response to fructose. Both high dietary fructose intake and elevated UA level may predict more severe hepatic ATP depletion in response to fructose and hence may be risk factors for the development and progression of NAFLD.

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