The Department of Nutrition

School of Health and Human Sciences











Michael K. McIntosh, Ph.D., R.D.

L. S. Keker Excellence Professor Emeritus
Curriculum Vitae

The long-term goal of Dr. Michael McIntosh’s research group is to develop dietary strategies to control human obesity, the most common nutritional disease in America. His group’s research seeks to provide a dietary approach instead of a drug approach to obesity management. Reductions in health problems and financial costs related to obesity would be expected.

The research, which utilizes human fat cells grown in culture as a cell model, focuses on two areas: 1) how increased body fat promotes insulin resistance observed in tpe 2 diabetes, and 2) identification of the mechanism(s) by which certain fatty acids and polyphenols affect cell signaling and the expression of genes and proteins that regulate fat cell maturation, metabolism, inflammation, and insulin resistance.

Fifty peer-reviewed publications in scientific journals and eight book chapters have resulted from Dr. McIntosh’s group’s work. External funding totals more than $4 million, including grants from the National Institutes of Health and the US Department of Agriculture. Students working with his lab group have won national research competitions (American Society of Nutrition, EB), fellowships (NIH NRSA F31s, ASN), and travel awards (Keystone, FASEB-MARC).


  • Ph.D., University of Georgia, 1987
  • M.S., University of Alberta, 1983
  • B.S., Ohio University, 1973

Research Interest

  1. Obesity, Inflammation, and Type 2 Diabetes:
    • How does increased adiposity promote inflammation and insulin resistance?
    • Role of gut microbiota in mediating or preventing inflammation and insulin resistance?
  2. Nutritional Regulation of Obesity, Inflammation, Intestinal Health, and Diabetes:
    •  Influence of an American-type diet on intestinal and systemic inflammation?
    •  Mechanism(s) by which California grapes prevent inflammation and insulin resistance?

Current Research

(using macrophages, adipocytes, and myotubes as cell models)

  • Anti-obesity mechanism of CLA isomer.
  • Anti-inflammatory role of bioactive components found in grapes and wine.
  • Pro-inflammatory capacity of cells isolated from human adipose tissue.

Recent Publications

(*= graduate students, # = undergraduate students)

  • Obsen,T.*, Faergeman, N.,Chung, S.*,Martinez, K., Gobern, S.#, Loreau, L, Wabitsch, Mandrup, S.,  M., McIntosh, M.  2012. Trans-10, cis-12 Conjugated Linoleic Acid Decreases de novo Lipid Synthesis in Human Adipocytes.  J. Nutr. Biochem. 23: 580-590.
  •  Reardon, M.#, Gobern, S.#, Martinez, K.*, Shen, W.*, Reid, T., McIntosh, M.  2012.  Oleic acid attenuates trans-10, cis-12 conjugated linoleic acid-mediated inflammatory gene expression in human adipocytes.  Lipids 47: 1043-1051.
  • Chuang, C-C.*, Shen, W.*, Chen, H.*, Xie, G., Jia, W., Chung, S., McIntosh, M.  2012. Differential effects of grape powder and its extract on glucose tolerance and chronic inflammation in high fat-fed obese mice.  J. Agric. Food Chem. 60: 12458-12468.
  • Martinez, K.*, S. Shyamasundar#, A. Kennedy*, C-C Chuang*, A. Marsh*, J. Kincaid, T.Reid, M. McIntosh. Diacylglycerol kinase inhibitor R59022 2013. Attenuates Conjugated Linoleic Acid-Mediated Inflammation in Human Adipocytes. J. Lipid Research. 54: 662-670
  • Shen, W*., Martinez, K.*, Chuang, C.*, Overman, A.*,  McIntosh, M.  2013. The Phospholipase C (PLC) Inhibitor U73122 Inhibits Trans-10, cis-12 Conjugated Linoleic Acid (10,12 CLA)-Mediated Inflammatory Signaling and Insulin Resistance in Human Adipocytes. J. Nutr. Mar. 6: (doi:10.3945/jn.112.173161)
  • Shen, W.*, Chuang, C.C.*, Martinez, K.*, Reid, T., Brown, J. M., Xi, L., Hixson, L.*, Hopkins, R., Starnes, J., McIntosh, M. 2013. Conjugated Linoleic Acid Reduces Adiposity and Increases Markers of Browning and Inflammation in White Adipose Tissue of Mice. J. Lipid Research. 54: 909-922.
  • Shen, W.*, Gaskins, H.R., McIntosh, M. 2014. Influence of dietary fat on intestinal microbes, inflammation, barrier function, and metabolic outcomes.  J. Nutr. Biochem. 25: 270-280.