SOM Faculty Profile : Heidi K Ortmeyer

Heidi K Ortmeyer

Heidi K Ortmeyer Ph.D.

Academic Title: Assistant Professor

Primary Appointment: Medicine

Secondary Appointments: Physiology

hortmeye@umaryland.edu

Location: Baltimore VA Medical Center, Room 4B-201A

Phone: (410) 605-7000 x5419

Fax: (410) 605-7913

Research Interests

Our laboratory is interested in understanding nutrient partitioning, especially triglyceride (TG) partitioning, and tissue-specific regulation of lipoprotein lipase (LPL), a key enzyme in TG metabolism. After a meal, plasma TG is broken down into fatty acids and glycerol by LPL, which is located within the capillary surrounding adipose tissue. The fatty acids are taken up by the adipose tissue and stored as TG until needed. During a fast, plasma TG is broken down into fatty acids and glycerol by the LPL located within the capillary surrounding muscle. The fatty acids are taken up by the muscle and oxidized for fuel or presumably stored as TG. What determines whether the fatty acids are oxidized or stored in muscle is unknown. However, these processes may play an important role in obesity and insulin resistance.

Recent studies by our laboratory show that adipose tissue LPL activity is reduced and skeletal muscle LPL activity is increased after weight loss and exercise in older, obese, postmenopausal women. Weight loss alone did not affect adipose tissue or skeletal muscle LPL activity, suggesting that exercise in conjunction with weight loss is a better method to “realign” tissue LPL activity. We have evidence from studies in nonhuman primates that the increase in skeletal muscle LPL activity after PPAR-a agonist treatment is positively associated with the increase in carnitine palmitoyltransferase (CPT) activity. CPT is the mitochondrial enzyme that allows long-chain fatty acids to be oxidized as fuel. In addition, the increase in CPT activity following PPAR-a agonist treatment is positively associated with the increase in glycogen synthase (GS) activity. GS is an important enzyme for glycogen storage. Therefore, we are interested in determining whether the increase in LPL activity following weight loss and exercise in postmenopausal women is associated with an increase in PPAR-a gene expression, an increase in CPT activity and/or an increase in GS activity in skeletal muscle. Our hypothesis is that an intervention that increases PPAR-a gene expression in skeletal muscle will improve fatty acid oxidation and therefore increase LPL activity (lower plasma TG) and increase GS activity (insulin sensitivity).

Publications

Most Recent Publications
Ferrara CM, AP Goldberg, HK Ortmeyer and AS Ryan. Effects of aerobic and resistive exercise trainingon glucose disposal and skeletal muscle metabolism in older men. J Gerontol A Biol Sci Med Sci, in press, 2006

Nadeau KJ, LB Ehlers, LE Aguirre, RL Moore, KN Jew, HK Ortmeyer, BC Hansen, JEB Reusch, B Draznin. Exercise training and calorie restriction increase SREBP-1 expression and intramuscular triglyceride in skeletal muscle. Am J Physiol Endocrinol Metab, in press 2006

Bodkin NL, HK Ortmeyer and BC Hansen. A comment on a comment: Relevance of nonhuman primate dietary restriction to aging in humans. J Gerontol A Biol Sci Med Sci 60:951-952, 2005

Ortmeyer HK, Y Adall, KR Marciani, A Katsiaras, AS Ryan, NL Bodkin and BC Hansen. Skeletal muscle glycogen synthase subcellular localization: effects of insulin and PPAR-alpha agonist (K-111) administration in rhesus monkeys. Am J Physiol Regul Integr Comp Physiol 288:R1509-R1517, 2005

Liao P, NL Bodkin, E Cho, T Alexander and HK Ortmeyer. Minimally invasive surgery via laparoscopy for intra-abdominal biopsy in obese rhesus macaques (Macaca mulatta). Comp Med 54:159-164, 2004

Bodkin NL, TM Alexander, HK Ortmeyer, E Johnson and BC Hansen. Mortality and morbidity in laboratory-maintained rhesus monkeys and effects of long-term dietary restriction. J Gerontol A Biol Sci Med Sci 58:212-219, 2003

Standaert, ML, HK Ortmeyer, MP Sajan, Y Kanoh, G Bandyopadhyay, BC Hansen and RV Farese. Skeletal muscle insulin resistance in obesity-associated type 2 diabetes mellitus in monkeys involves a defect in insulin activation of atypical protein kinase-C. Diabetes 51:2936-2943, 2002

Pender, C, HK Ortmeyer, BC Hansen, ID Goldfine and JF Youngren: Elevated plasma cell membrane glycoprotein levels and diminished insulin receptor autophosphorylation in obese, insulin-resistant rhesus monkeys. Metabolism 51:465-470, 2002

Shashkin PN, HK Wasner, HK Ortmeyer and BC Hansen: Prostaglandylinositol cyclic phosphate (cPIP): a novel second messenger of insulin action. Comparative analysis of two kinds of 'insulin mediators'. Diabetes Metab Res Rev 17:273-84, 2001

Shashkin PN, T Meckmongkol, HK Wasner, BC Hansen and HK Ortmeyer: Prostaglandylinositol cyclic phosphate synthase activity in the liver of insulin-resistant rhesus monkeys before and after a euglycemic hyperinsulinemic clamp. J Basic Clin Physiol Pharmacol 12:1-18, 2001

Hotta, K., Funahashi, T., Bodkin, N. L., Ortmeyer, H. K., Arita, Y., Hansen, B. C., Matsuzawa, Y. Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys. Diabetes 50:1126-1133, 2001

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