Purnell JQ, Klopfenstein BA, Stevens AA, Havel PJ, Adams SH, Dunn TN, Krisky C, Rooney WD.

Department of Medicine, Oregon Health & Science University, Portland, OR, USA. purnellj@ohsu.edu

Abstract
AIMS: In animals, intracerebroventricular glucose and fructose have opposing effects on appetite and weight regulation. In humans, functional brain magnetic resonance imaging (fMRI) studies during glucose ingestion or infusion have demonstrated suppression of hypothalamic signalling, but no studies have compared the effects of glucose and fructose. We therefore sought to determine if the brain response differed to glucose vs. fructose in humans independently of the ingestive process.

METHODS: Nine healthy, normal weight subjects underwent blood oxygenation level dependent (BOLD) fMRI measurements during either intravenous (IV) glucose (0.3 mg/kg), fructose (0.3 mg/kg) or saline, administered over 2 min in a randomized, double-blind, crossover study. Blood was sampled every 5 min during a baseline period and following infusion for 60 min in total for glucose, fructose, lactate and insulin levels.

RESULTS: No significant brain BOLD signal changes were detected in response to IV saline. BOLD signal in the cortical control areas increased during glucose infusion (p = 0.002), corresponding with increased plasma glucose and insulin levels. In contrast, BOLD signal decreased in the cortical control areas during fructose infusion (p = 0.006), corresponding with increases of plasma fructose and lactate. Neither glucose nor fructose infusions significantly altered BOLD signal in the hypothalamus.

CONCLUSION: In normal weight humans, cortical responses as assessed by BOLD fMRI to infused glucose are opposite to those of fructose. Differential brain responses to these sugars and their metabolites may provide insight into the neurologic basis for dysregulation of food intake during high dietary fructose intake.

© 2011 Blackwell Publishing Ltd.

Ramdas WD, Wolfs RC, Hofman A, de Jong PT, Vingerling JR, Jansonius NM.
Wolfs, Hofman, Vingerling, and Jansonius) and Ophthalmology (Drs Ramdas, Wolfs, and Vingerling), Erasmus Medical Center, Rotterdam, Department of Ophthalmogenetics, the Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences (Dr de Jong), and Department of Ophthalmology, Academic Medical Center (Dr de Jong), Amsterdam, and Department of Ophthalmology, University Medical Center Groningen, University of Groningen, Groningen (Dr Jansonius).
Abstract
OBJECTIVE: To determine whether lifestyle-related risk factors, such as socioeconomic status, smoking, alcohol consumption, and obesity, are associated with open-angle glaucoma (OAG).
METHODS: Participants from the Rotterdam Study, a prospective population-based cohort study, were considered eligible if they participated at both baseline and follow-up and if they had no OAG at baseline. All participants underwent an identical ophthalmologic examination at all visits, including intraocular pressure measurements, optic nerve head assessment, and perimetry. Lifestyle-related factors were assessed by questionnaires by trained research assistants or measured during the examinations (body mass index and waist to hip ratio). Cox proportional hazard regression analysis was applied to calculate hazard ratios.
RESULTS: Of 3939 eligible participants, 108 (2.7%) developed OAG during 9.7 years’ mean follow-up. No statistically significant effect of socioeconomic status, smoking, or alcohol intake was found. In women, each unit increase in body mass index resulted in a 7% decrease in the risk of developing OAG (P = .04). There was a significant increasing effect of body mass index on intraocular pressure (P < .001) in women.
CONCLUSIONS: Obesity appears to be associated with a higher intraocular pressure and a lower risk of developing OAG. These associations were only present in women. Other lifestyle-related factors, such as socioeconomic status, smoking, and alcohol consumption, were not associated with OAG.

Zemel MB, Richards J, Mathis S, Milstead A, Gebhardt L, Silva E.

Department of Nutrition, The University of Tennessee, Knoxville, TN 37996-1920, USA. mzemel@utk.edu

Int J Obes (Lond). 2005 Apr;29(4):391-7. Links