Cary Mariash

Curriculum Vitae (pdf)
Professor of Medicine

M.D. Degree: University of California, San Diego, California
Residency Training: University of Minnesota, Minneapolis, MN.
Fellowship Training: University of Minnesota, Minneapolis, MN.
Clinical Specialty: General Endocrinology and Thyroid Disease
Primary Research Interest: Nutritional regulation of gene expression, thyriod hormone.

Email: mariasc@umn.edu

Research interests:

My research program is primarily involved in understanding the mechanisms by which changes in thyroid hormone or dietary sugar change the expression of genes involved in lipid synthesis. Both an increase in thyroid hormone levels and an increase in the consumption of dietary sucrose stimulate the genes that produce long chain fatty acids in the liver and in fat. Both these factors interact synergistically to regulate these genes. In the absence of thyroid hormone, dietary sugars can not effectively induce the lipogenic enzyme genes. Similarly, in fasted animals the administration of thyroid hormone is associated with markedly decreased response of these genes. An understanding of the regulation of this system will allow us to develop strategies to effectively treat diseases such as obesity or prevent complications from diseases associated with metabolic dysfunction such as diabetes mellitus. We use a number of different molecular biologic techniques to study the mechanisms that regulate these genes. Some of these techniques include the transfer of artificial genes into primary liver cells, isolation and purification of transcription factors, cDNA and genomic cloning, transgenic animal studies, and gene disruption techniques to create gene "knockout" animals.

The laboratory is also engaged in understanding the mechanisms by which thyroid hormone regulates brain development. Humans with insufficient thyroid hormone during fetal and early neonatal development suffer from various degrees of mental retardation. In the most severe form it is called cretinism. The laboratory is using similar molecular biologic techniques as described above to study the regulation of brain development by thyroid hormone. We are studying how thyroid hormone and thyroid hormone receptors regulate the differentiation of precursor nueronal cells into mature neuronal cell types such as the myelin producing oligodendroglia cell and the cerebellar Purkinje cell.

Recent Publications:

1. Ota, Y. and C.N. Mariash, Paradoxical triiodothyronine suppression of S14 transcription in permanent hepatic cell lines. Thyroid, 2003. 13 (5): p. 437-45.
2. Lei, J., et al., Thyroid hormone stimulates Na-K-ATPase activity and its plasma membrane insertion in rat alveolar epithelial cells. Am J Physiol Lung Cell Mol Physiol, 2003. 285 (3): p. L762-72.
3. Jones, S.A., et al., Triiodothyronine is a survival factor for developing oligodendrocytes. Mol Cell Endocrinol, 2003. 199 (1-2): p. 49-60.
4. Campbell, M.C., G.W. Anderson, and C.N. Mariash, Human Spot 14 Glucose and Thyroid Hormone Response: Characterization and TRE Identification. Endocrinology, 2003.
5. Zhu, Q., et al., Spot 14 gene deletion increases hepatic de novo lipogenesis. Endocrinology, 2001. 142 (10): p. 4363-70.
6. Sunil, G.S. and C.N. Mariash, Hashimoto's encephalitis. J Clin Endocrinol Metab, 2001. 86 (2): p. 947.
7. Zhu, X.G., et al., The orphan nuclear receptor Ear-2 is a negative coregulator for thyroid hormone nuclear receptor function. Mol Cell Biol, 2000. 20 (7): p. 2604-18.
8. Ercan-Fang, S., et al., Quantitative assessment of pituitary resistance to thyroid hormone from plots of the logarithm of thyrotropin versus serum free thyroxine index. J Clin Endocrinol Metab, 2000. 85 (6): p. 2299-303.
9. Liu, B., W. Li, and C.N. Mariash, Two different gene elements are required for glucose regulation of S14 transcription. Mol Cell Endocrinol, 1999. 148 (1-2): p. 11-9.
10. Kirschner, L.S. and C.N. Mariash, Adipose S14 mRNA is abnormally regulated in obese subjects. Thyroid, 1999. 9 (2): p. 143-8.
11. Sandhofer, C., et al., Beta receptor isoforms are not essential for thyroid hormone-dependent acceleration of PCP-2 and myelin basic protein gene expression in the developing brains of neonatal mice. Mol Cell Endocrinol, 1998. 137 (2): p. 109-15.
12. Anderson, G.W., et al., Chicken ovalbumin upstream promoter-transcription factor (COUP-TF) modulates expression of the Purkinje cell protein-2 gene. A potential role for COUP-TF in repressing premature thyroid hormone action in the developing brain. J Biol Chem, 1998. 273 (26): p. 16391-9.
13. Ota, Y., et al., Cloning, expression and regulation of the human S14 gene. Mol Cell Endocrinol, 1997. 126 (1): p. 75-81.
14. Anderson, G.W., et al., Purkinje cell protein-2 cis-elements mediate repression of T3-dependent transcriptional activation. Mol Cell Endocrinol, 1997. 131 (1): p. 79-87.
15. Sudo, Y. and C.N. Mariash, Lowering glucose depletes a thapsigargin-sensitive calcium pool and inhibits transcription of the S14 gene. Endocrinology, 1996. 137 (11): p. 4677-84.
16. Harmon, J.S. and C.N. Mariash, Identification of a carbohydrate response element in rat S14 gene. Mol Cell Endocrinol, 1996. 123 (1): p. 37-44.