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Andrew P Goldberg
 

Andrew P Goldberg M.D.

Academic Title: Professor
Primary Appointment: Medicine
Secondary Appointments: Family & Community Medicine
Administrative Title: Division Head
agoldber@medicine.umaryland.edu
Location: Howard Hall, 115
Phone: 410-706-6052
Fax: 410-706-6053

Personal History:

Dr. Goldberg leads research programs funded by NIH 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.

The Goldberg laboratory examines the mechanisms by which exercise and weight loss affect obesity and its glucose and lipid metabolic complications. His studies show 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 work shows that mechanisms in both adipose tissue and muscle contribute to the metabolic complications associated with central obesity and are modifiable by exercise and weight loss by increasiing lipid oxidation in muscles and reducing storage in adipose tissue. His current research assesses the cellular mechanisms by which weight loss and exercise improve adipose and muscle metabolism in obesity, where the addition of a moderate intensity exercise to weight loss partitions 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 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.

Research Interests:

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.

The Goldberg laboratory examines the mechanisms by which exercise and weight loss affect obesity and its glucose and lipid metabolic complications. His studies show 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 work shows that mechanisms in both adipose tissue and muscle contribute to the metabolic complications associated with central obesity and are modifiable by exercise and weight loss. His 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 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.


Publications:

Selected Publications

Luft AR, Macko RF, Forrester LW, Villagra F, Ivey F, Sorkin JD, Whitall J, McCombe-Waller S, Katzel L, Goldberg AP, Hanley DF.  Treadmill exercise activates subcortical neural networks and improves walking after stroke: A randomized controlled trial.  Stroke 2008;39:3341-3350.  PMCID: PMC2929142  

Fried SK, Tittelbach T, Blumenthal J, Sreenivassan U, Robey L, Yi J, Khan S, Hollender C, Ryan AS, Goldberg AP.  Resistance to the antilipolytic effect of insulin in adipocytes of African-Americans compared to Caucasian post-menopausal women.  J Lipid Res 2010;51:1193-1200.  PMCID:  PMC2853446

Joseph LJ, Prigeon RL, Blumenthal JB, Ryan AS, Goldberg AP.  Weight loss and low-intensity exercise for  the treatment and prevention of metabolic syndrome in obese postmenopausal women.  J Gerontol 2011;66A:M1022-M1029.  PMCID: PMC3156630

Brinkley TE, Halverstadt A, Phares DA, Ferrell RE, Prigeon RL, Hagberg JM, Goldberg AP.  Hepatic lipase gene -514C>T variant is associated with exercise training-induced changes in VLDL and HDL by lipoprotein lipase.  J Appl Physiol 2011;111:1871-1876. PMCID: PMC3233892

Supiano M, Alessi C, Chernoff R, Goldberg A, Morley J, Schmader K, Shay K.  VA Geriatric Research, Education and Clinical Centers: Translating aging research into clinical geriatrics; also Appendix S1.  J Amer Geriatr Soc 2012;60:1347-1356.

Hanson ED, Sheaff AK, Sood S, Ma L, Francis JD, Goldberg AP, Hurley BF.  Strength training induces muscle hypertrophy and functional gains in black prostate cancer patients despite androgen deprivation therapy.  J Gerontol A Biol Sci Med Sci. 2013 Apr;68(4):490-8. Epub 2012 Oct 22.  PMCID: PMC3593619.

Ryan AS, Katzel LI, Prior SJ, McLenithan JC, Goldberg AP, Ortmeyer HK.  Aerobic Exercise Plus Weight Loss Improves Insulin Sensitivity and Increases Skeletal Muscle Glycogen Synthase Activity in Older Men.  J Gerontol A Biol Sci Med Sci. 2013 Dec 19. [Epub ahead of print]  PMID:  24357038 [PubMed - as supplied by publisher]

Prior SJ, Ryan AS, Stevenson TG, Goldberg APMetabolic inflexibility during submaximal aerobic exercise is associated with glucose intolerance in obese older adults.  Obesity (Silver Spring). 2014 Feb;22(2):451-7. doi: 10.1002/oby.20609. Epub 2013 Oct 16.  PMID:  23983100 [PubMed - in process]

Prior SJ, Blumenthal JB, Katzel LI, Goldberg AP, Ryan AS.  Increased Skeletal Muscle Capillarization After Aerobic Exercise Training and Weight Loss Improves Insulin Sensitivity in Adults With IGT.  Diabetes Care. 2014 May;37(5):1469-75. doi: 10.2337/dc13-2358. Epub 2014 Mar 4. PMID: 24595633 [PubMed - in process]

Sorkin JD, Vasaitis TS, Streeten E, Ryan AS, Goldberg APEvidence for threshold effects of 25-hydroxyvitamin D on glucose tolerance and insulin resistance in black and white obese postmenopausal women.  J Nutr. 2014 May;144(5):734-42. doi: 10.3945/jn.114.190660. Epub 2014 Apr 9.  PMID: 24717362  [PubMed - in process]

Halter J,  Musi N, Horne , Crandall J, Goldberg A, Harkless L, Hazzard W, Huang E, Kirkman MS, Plutzky J, Schmader K, Zieman S, High K.  Diabetes Mellitus and Cardiovascular Disease in Older Adults: Current Status and Future Directions.  Diabetes 2014 ;63:2578-2589