Obesity and its negative impacts on health – including metabolic syndrome, type-2 diabetes mellitus and cardiovascular complications are a global pandemic 1 and defining ailments of our era. The worldwide incidence of obesity has more than doubled since 1980, and in 2014 more than 1.9 billion adults were overweight – and of these, 600 million were obese 2. Currently, the mechanisms that govern healthy adipose tissue expansion versus those at play in obesity-driven syndromes remain poorly understood. During weight gain in response to excessive caloric intake, lipid overload in adipose tissue triggers classical macrophage polarization, cytokine release, systemic inflammation and recruitment of infiltrating adipose tissue macrophages (ATMs), which in concert are believed to contribute to systemic complications such as insulin resistance 3-5.
Our lab is interested in 2 fundamental questions:
1- What are the mechanisms involved in healthy adipose tissue expansion and how do they become deregulated in disease?
2- By what mechanisms does increased adiposity contribute to distal diseases such as retinopathies and AMD.
REFERENCES
- Taubes, G. Insulin resistance. Prosperity’s plague. Science 325, 256-260 (2009).
- World Health Organisation, W.H.O., Vol. 2016 (2015).
- Weisberg, S.P. et al. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest 112, 1796-1808 (2003).
- Kanda, H. et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest 116, 1494-1505 (2006).
- Olefsky, J. & Glass, C. Macrophages, inflammation, and insulin resistance. Annual Review of Physiology 72, 219-246 (2010).
Sapieha Lab 