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Minnesota Obesity Center

2000 Grant Awards

Is the Proximity to Commercial Food Outlets Related to Eating Behavior and Body Mass Index?

Maureen McGuire, Ph.D.
Division of Epidemiology, Univerity of Minnesota

The dramatic increase in obesity over the past few decades is almost certainly due to rapidly evolving environmental factors that affect energy intake and expenditure. The term "toxic environment" has been used to describe environmental changes (e.g., technological advances, automation, television, and the proliferation of commercial food outlets) that may be promoting decreases in physical activity and increases in dietary intake. However, few studies have evaluated the physical environmental factors related to obesity and obesity-related behaviors and none have considered the potential of food outlet proliferation on eating behavior.

The primary objective of the proposed research is to evaluate the relationship between the number of commercial food outlets within a given radius of individuals' homes and workplaces and eating behaviors (e.g., eating at commercial food outlets, calorie-intake, and fat-intake) and body mass index (BMI). It is hypothesized that the number of commercial food outlets within a given radius of people's homes and workplaces will be positively correlated to the frequency of eating at commercial food outlets, calorie-intake, fat intake, and BMI.

 

The Quantification of Fatty Acid and Glucose Turnover in Rodents: Effects of the Absence of Adipose Tissue Fatty Acid Binding Protein.

Elizabeth J. Parks, Ph.D.
Department of Food Science and Nutrition, University of Minnesota

The proposed experiments are designed to establish a method for the measurement of substrate turnover in mice and then use the method to determine whether a mouse strain lacking adipose tissue fatty acid binding protein (the ALBP/aP2 -/- mouse) has reduced absolute NEFA turnover. Twelve-week old control and genetically altered male mice (n=12 in each group) who have been fed a high-fat diet from weaning, will undergo a 3h metabolic infusion of stable isotopes to quantify de novo lipid synthesis and non-esterified fatty acid (NEFA). Glucose and glycerol flux will also be measured. We hypothesize that de novo fatty acid synthesis and glucose turnover will be upregulated, against a background of reduced NEFA flux. The experiments can set the stage for future studies investigating the impact of fatty acid flux on obesity-induced insulin resistance.

Currently, data from transgenic and knockout mouse studies include the comprehensive identification of which genes and/or proteins are up- and down-regulated at a single timepoint. The present project will establish methodology to measure the flux of numerous metabolites, simultaneously resulting from genetic manipulation. In the future, the combination of molecular data and metabolic mechanisms will greatly expand our understanding of how multiple systems are organized to result in what we observe as the "phenotype" of obesity-linked disease.

Recipients of:

2010 Grant Awards
2008 Grant Awards
2006 Grant Awards
2004 Grant Awards
2003 Grant Awards
2002 Grant Awards
2001 Grant Awards
2000 Grant Awards
1999 Grant Awards
1998 Grant Awards
1997 Grant Awards
1996 Grant Awards
1995 Grant Awards

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