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[body] => [<div class="field field-type-image field-field-people-image"><div class="field-label">People Image: </div><div class="field-items"><div class="field-item"><img src="http://www.diabetescenters.org/files/AGoldberg.jpg" alt="AGoldberg.jpg" title="AGoldberg.jpg" width="200" height="250" /></div></div></div><div class="field field-type-text field-field-center-name"><div class="field-label">Center Name: </div><div class="field-items"><div class="field-item">DRTC - Johns Hopkins University/University of Maryland</div></div></div><div class="field field-type-text field-field-core"><div class="field-label">Core List: </div><div class="field-items"><div class="field-item">DRTC Baltimore Clinical Investigation Core</div></div></div><div class="field field-type-text field-field-phone-number"><div class="field-label">Phone Number: </div><div class="field-items"><div class="field-item">410-605-7183</div></div></div><div class="field field-type-text field-field-people-details"><div class="field-label">People Details: </div><div class="field-items"><div class="field-item"><p><span id="lblResearchInterests"><font size="2">Dr. Goldberg leads research programs in the Baltimore VA GRECC, NIH RO1 grants and UMB Claude D. Pepper Older American Independence Center that investigate the hypothesis that some of the functional declines and medical diseases associated with aging in Western society are contributed to significantly by physical deconditioning and the development of obesity, i.e. lifestyle habits, as well as genetic and ethnic factors, not aging per se. Aging and obesity have many medically-related similarities, and there is a progressive relationship between obesity, physical deconditioning and risk for diabetes, hypertension, hyperlipidemia and their arteriosclerotic-thrombotic complications.<br /> <br />The Goldberg laboratory examines the mechanisms by which exercise and weight loss affect obesity and its glucose and lipid metabolic complications. Our previous studies show that weight loss is more effective than exercise in improving glucose and lipid metabolism and blood pressure profiles in obese older men and women, and that the combined effects of exercise and weight loss are synergistic in reducing central obesity and raising VO2 max to reduce CVD risk factors associated with the metabolic syndrome. These and other studies confirm that exercise and weight loss increase insulin sensitivity and reduce lipid profiles, hyperinsulinemia and glucose intolerance more than either do independently in obese men and women. This suggests that mechanisms in both adipose tissue and muscle contribute to the metabolic complications associated with central obesity and may be modifiable by exercise and weight loss. Current research assesses the cellular mechanisms by which weight loss and exercise improve the metabolic dysfunction associated with obesity. The addition of a moderate intensity exercise to weight loss seems to partition nutrients to muscle for oxidation, in contrast to weight loss alone which does not increase lipoprotein lipase, the rate limiting enzyme for lipid uptake by muscle. The influence of gene polymorphisms (LPL, PPAR) on metabolic and body fat responses to weight loss and exercise training are being studied to test the hypothesis that obese subjects with certain certain gene variants may respond better to exercise than weight loss.</font></span></p>
<p><a href="http://medschool.umaryland.edu/facultyresearchprofile/viewprofile.aspx?id=495"><span><font size="2">More</font></span></a></p>
</div></div></div><div class="field field-type-text field-field-center-title"><div class="field-label">center_title: </div><div class="field-items"><div class="field-item">Director, Clinical Investigation Core</div></div></div>]
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[value] => [<p><span id="lblResearchInterests"><font size="2">Dr. Goldberg leads research programs in the Baltimore VA GRECC, NIH RO1 grants and UMB Claude D. Pepper Older American Independence Center that investigate the hypothesis that some of the functional declines and medical diseases associated with aging in Western society are contributed to significantly by physical deconditioning and the development of obesity, i.e. lifestyle habits, as well as genetic and ethnic factors, not aging per se. Aging and obesity have many medically-related similarities, and there is a progressive relationship between obesity, physical deconditioning and risk for diabetes, hypertension, hyperlipidemia and their arteriosclerotic-thrombotic complications.<br /> <br />The Goldberg laboratory examines the mechanisms by which exercise and weight loss affect obesity and its glucose and lipid metabolic complications. Our previous studies show that weight loss is more effective than exercise in improving glucose and lipid metabolism and blood pressure profiles in obese older men and women, and that the combined effects of exercise and weight loss are synergistic in reducing central obesity and raising VO2 max to reduce CVD risk factors associated with the metabolic syndrome. These and other studies confirm that exercise and weight loss increase insulin sensitivity and reduce lipid profiles, hyperinsulinemia and glucose intolerance more than either do independently in obese men and women. This suggests that mechanisms in both adipose tissue and muscle contribute to the metabolic complications associated with central obesity and may be modifiable by exercise and weight loss. Current research assesses the cellular mechanisms by which weight loss and exercise improve the metabolic dysfunction associated with obesity. The addition of a moderate intensity exercise to weight loss seems to partition nutrients to muscle for oxidation, in contrast to weight loss alone which does not increase lipoprotein lipase, the rate limiting enzyme for lipid uptake by muscle. The influence of gene polymorphisms (LPL, PPAR) on metabolic and body fat responses to weight loss and exercise training are being studied to test the hypothesis that obese subjects with certain certain gene variants may respond better to exercise than weight loss.</font></span></p><p><a href="http://medschool.umaryland.edu/facultyresearchprofile/viewprofile.aspx?id=495"><span><font size="2">More</font></span></a></p>]
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<p><a href="http://medschool.umaryland.edu/facultyresearchprofile/viewprofile.aspx?id=495"><span><font size="2">More</font></span></a></p>
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<p><a href="http://medschool.umaryland.edu/facultyresearchprofile/viewprofile.aspx?id=495"><span><font size="2">More</font></span></a></p>
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<p><a href="http://medschool.umaryland.edu/facultyresearchprofile/viewprofile.aspx?id=495"><span><font size="2">More</font></span></a></p>
</div></div></div><div class="field field-type-text field-field-center-title"><div class="field-label">center_title: </div><div class="field-items"><div class="field-item">Director, Clinical Investigation Core</div></div></div>]
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