Pauline Koh-Banerjee

Defining Risks for Diabetes

While gaining weight may seem an inevitable byproduct of aging as metabolism slows, eating and exercise habits change, and muscle mass decreases, the added pounds may have serious health effects.

Pauline Koh-Banerjee, doctoral student in the Department of Nutrition, presented "Changes in Body Weight and Fat Distribution as Risk Factors for Clinical Diabetes in US Men" at HSPH’s Poster Day. Other members of the research team were Youfa Wang of the University of Chicago; HSPH professors Donna Spiegelman and Walter Willett; and HSPH associate professors Frank Hu and Eric Rimm.

The team investigated the role of weight gain and weight distribution and the risk of diabetes among 22,219 men between ages 40 and 75 who were enrolled in the Health Professionals’ Follow-Up Study. Long-term weight gain was calculated as the difference between self-reported weight in 1996 and recalled weight at age 21.

For every kilogram of weight gained, the risk for diabetes increased by seven percent. Men with the highest body mass index at age 21 and with the greatest weight gain between age 21 and age reached by 1996 had 17.4 times the risk of diabetes compared to men who were leanest at age 21 and who had gained the least weight.

Even if weight remained relatively steady, men whose waistlines expanded were at increased risk for diabetes. In other words, where fat ends up getting deposited on the body appears to matter. The scientists calculated that 17 percent of the cases of diabetes that emerged in the cohort could have been avoided if the men had added less than 1 inch to their waistlines over nine years.

The research is the first prospective study to report the association between changes in fat distribution and diabetes incidence.

The scientists also found that decrease in hip girth was associated with increased risk for diabetes. They hypothesized that the risk may be associated with loss of lean muscle mass.

Making Headway in Leukemia Research

The anti-tumor protein p53 is mutated or missing in many kinds of cancer, but in leukemia, the situation is puzzlingly different. The protein is intact and present. Something must be interfering with p53’s function, scientists have hypothesized.

	Dmitri Wiederschain

The team is now investigating ways to disrupt the binding between p53 and MLL-ELL, which could help lead to improved leukemia treatment.

Approximately 29,000 adults and 2,000 children are diagnosed with leukemia each year in the U.S., according to the National Cancer Institute.

Randi Paynter, Department of Epidemiology
"CYP19 Gene Polymorphisms and Endometrial Cancer Risk"

Michelle Soriano, Department of Immunology and Infectious Diseases
"SLIM, a Novel Negative Regulator of STAT Function during Type I Immunity"

Aeisha Dominique Robb, Department of Nutrition
"Transferrin Receptor 2 Expression is Associated with a Biphasic Pattern of Transferring Uptake and Redistribution of Transferring to Multivescular Bodies"

Yi Kyung Park, Department of Nutrition
"Dietary Fiber and Risk of Colorectal Cancer: A Pooled Analysis of Cohort Studies"

Elizabeth Heilig, Department of Cancer Cell Biology
"Metal Transport across the Pulmonary Epithelium: A Regulated Process"