Dr. Josiane Broussard

As a Branco Weiss fellow, Dr. Josiane Broussard is working to examine the links between sleep restriction and/or disruption and the development of insulin resistance, increased circulating free fatty acids and diabetes.

Background

Born

USA

Studies

Josiane's postgraduate research focused on elucidating the mechanisms linking sleep and obesity. In particular, she examined the effects of sleep restriction in healthy young volunteers on insulin sensitivity in adipocytes, as well as 24-hour profiles of circulating hormones.

  • Postdoctoral Scientist at Cedars-Sinai Medical Center, Los Angeles, California, USA
  • PhD in Molecular Metabolism and Nutrition at the University of Chicago, Chicago, Illinois, USA 2010
  • Postgraduate studies in the Neurology Department, Harvard University and Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA 2002-2004
  • Undergraduate studies in Neuroscience at Brandeis University, Waltham, Massachusetts, USA 2002

Major Awards

  • Sleep Research Society Young Investigator Award 2013
  • Naomi Berrie Diabetes Fellow; Mentor: Dr. Richard Bergman, Ph.D., University of Southern California 2009-2011
  • University of Chicago, Outstanding Performance Award in the field of Molecular Metabolism and Nutrition 2010
  • 11th International Sleep and Breathing Symposium Anne Elizabeth Suratt Young Investigator Award 2009
  • Sleep Research Society Abstract Excellence Award 2009
  • Sleep Research Society Meritorious Abstract Award 2008

In the News

Lack of sleep can seriously affect metabolism, Los Angeles Times 2012

The Science Of Sleep: 60 Minutes, CBSNews 2009

Naomi Berrie Fellow, Columbia University Press Release 2009

Weighing effects of too little sleep, Chicago Tribune 2006

 

Research

Society in Science Fellow Since

2011

Research Category

Biomedical Sciences

Research Location

Diabetes and Obesity Research Institute, Biomedical Sciences, Cedars-Sinai Medical Center, USA

Background

Everything cycles through periods of rest and activity, from worms to flies to cells. Sleep possesses distinct stages; however its function remains a mystery. Only humans voluntarily curtail their sleep for non-life-threatening reasons. Loss of sleep quantity and/or quality occurs due to behavioral sleep curtailment, normal healthy aging, as well as sleep disorders such as insomnia. Many diseases are associated with reduced sleep duration including heart disease, hypertension, mood disorders, inflammatory diseases, diabetes and obesity.

Between 1960 and 2000 there has been a marked increase in the prevalence of obesity in the United States, as well as a steady rise in diabetes.  In the same time period, sleep hours have declined on average by 1.5 hours per person. Although changes in diet and exercise have clearly played an important role, reduced sleep duration and quality is another possible factor in this diabetic epidemic. Obesity and diabetes, with both their health and economic consequences, are global problems. It is crucial therefore, to identify modifiable causes as potential areas of intervention.

Details of Research

Studies indicate that reduced sleep duration and/or quality results in decreased glucose tolerance, reduced insulin secretion, impaired insulin action and decreased leptin levels. It is likely that the adverse impact of sleep loss on glucose metabolism and leptin levels involves multiple pathways. These include reduced glucose tolerance due to reduced brain glucose utilization, reduced insulin release due to increased sympathovagal balance at the level of the pancreatic beta-cell, reduced insulin sensitivity due to higher evening cortisol levels, lower leptin secretion due to impaired insulin signaling and increased sympathovagal balance at the level of the adipocytes.

Josiane's research examines the links between sleep and health in an animal model with the hope of uncovering mechanisms by which poor sleep can result in insulin resistance and diabetes risk.  This model will allow further investigation of the mechanisms involved in sleep restriction-induced insulin resistance.