Dr. Philip Wood is immersed in fat: fat metabolism, fatty acids, fat signaling, fatty liver disease. Dr. Wood, a professor in the Metabolic Signaling and Disease program at Sanford-Burnham’s Lake Nona campus, is trying to unravel the consequences of too much fat.
“I’m interested in how the body reacts to excess fat and how fat metabolism and the genetics of fat metabolism play a role in insulin resistance and fatty liver disease,” says Dr. Wood.
Given that recent statistics show a third of Americans are obese, the research being done by Dr. Wood and others could have a profound impact on the nation’s health. One key focus is the underlying genetics that make certain people susceptible to disease.
“We’re not going to find specific genes that cause type 2 diabetes,” says Dr. Wood. “Perhaps they exist in rare cases, but not enough for a genetic risk assessment. We’re not looking for the cause of the disease; we’re looking at the body’s response to this burden of excess fat. We’re asking: Why do some people have a predisposition towards insulin resistance in the face of obesity? So we’re looking at the genetics of response, not the genetics of cause.”
Dr. Wood is developing mouse models to evaluate insulin sensitivity and its correlation with enzyme deficiency. He notes that many researchers have used the leptin-deficient mouse to study diabetes. Leptin is a hormone that regulates appetite and metabolism, and mice with reduced leptin are prone to obesity. But they are not the model Dr. Wood is looking for.
“Leptin-deficient mice weigh three times as much as a normal mouse,” says Dr. Wood. “So if you translate that into humans, we’re talking 400 or 500 pounds. That’s fine, if you’re studying morbid obesity, but we’re interested in a model that’s more moderate, like what we would commonly find in people.”
By developing more precise models, Dr. Wood hopes to tease out the various genetic traits that make up the complex trait of type 2 diabetes. For example, a particular gene might contribute 20 percent to insulin resistance. How does that gene combine with other genes to create the larger trait?
“We want to use models where fat metabolism has been disrupted to characterize these traits,” says Dr. Wood. “We want to see if we can put a genetic print to that. That’s the only way we’ll be able to use genetic biomarkers to predict risk.”
The snacking right has dentfiiely helped me. I eat something small, like an apple of a fiber bar between meals to keep the metabolism going, and my weight has steadily dropped. (I exercise, too, so I can’t say the food’s everything, but it does help.)
Hi Kenneth:
l have a big challenge for you? l6 months ago l developed a horrific disease Dercums Stage 11. l was astonished, l’d been a health nut since my 30′s. l’m now 67, female.It’s a fatty Rheumatism, limpoma disorder, your body just growsfat, it’s unbearable. 30 HMO doctors couldn’t diagnose me, they did a 7 inch biopsy on my arm, the worst thing for this disease, now dozens of limpomas appeared where they cut. It also caused systemic Lymphedema?l have to wear compression garments for the rest of my life, on my arms, my legs, torso.
l ransacked the internet and found a test called Darkfield Microscopy, l did this test and it came up with the possibility of Dercums Disease. No cure, progressive. l keep searching and writing to doctors to find an answer, even though there doesn’t seem to be one. l found Karen L.Herbst.MD, Ph.D. She’s not much help?l’m becoming obese, ln 6 months l’ve gained 50 lbs. lt’s terrifying me.
You can watch a 4 min. video on Dercums, YouTube Dercums Disease Explained.
Thank you for writing back if you do?
Lynette May949 498 9770
how can u correlate obesity with hypothyrodism or what is their affect on humans
Hypothyroidism is a condition in which the thyroid doesn’t manufacture enough hormones. There are many reasons a thyroid might be underactive, but the end result is the same – the body’s normal chemical balance is disrupted. Weight gain is a common symptom, but the cause-effect relationship between hypothyroidism and clinical obesity is unclear. While hypothyroidism isn’t specifically a main focus of Sanford-Burnham’s research, perhaps our findings in metabolism and obesity will one day help shed more light on this condition.