Why underweight babies become obese: Study says disrupted hypothalamus is to blame

ScienceDaily (May 2, 2012) — It seems improbable that a baby born underweight would be prone to obesity, but it is well documented that these children tend to put on weight in youth if they're allowed free access to calories. Now, researchers believe they understand why this happens.

See Also:Health & MedicineObesityDiet and Weight LossInfant's HealthFitnessDiseases and ConditionsPregnancy and ChildbirthReferenceAppetiteBirth weightInfantNutrition and pregnancy

A new animal model study at UCLA has found that in low-birth-weight babies whose growth was restricted in the womb, the level of appetite-producing neuropeptides in the brain's hypothalamus -- the central control of the appetite -- is higher, resulting in a natural tendency among these children to consume more calories.

"Other studies have shown that neuronal processes that signal the brain to eat were wired differently in the hypothalamus if a hormonal gene, such as leptin, was missing," said the study's lead author, Dr. Sherin Devaskar, professor of pediatrics and executive chair of the department of pediatrics at Mattel Children's Hospital UCLA. "What we found is that appetite-producing genes in the hypothalamus are completely programmed toward eating more to make up for the relative decrease in nutrition while in the womb. So the natural tendency for a child born with low birth weight is to eat more and try to catch up in growth. But if this is not curbed, it can result in childhood obesity."

The findings appear in the June issue of the Journal of Neuroscience Research and are currently available online.

The study was undertaken in rodent models that mimicked small human babies. This was accomplished by reducing rodent mothers' intake of calories, which in turn led to the birth of small, low-birth-weight and growth-restricted babies. The rodent babies were then examined at an early age to see how much milk they consumed and to monitor their energy expenditure. In addition, the researchers examined the effect that being growth-restricted in the womb had on hypothalamic neuropeptides that control appetite when the babies were weaned.

The researchers observed that those neuropeptides that bring increased appetite with decreased energy expenditure were increased in the hypothalamus, while the neuropeptides that reduce appetite and increase energy expenditure were decreased. Therefore, the homeostatic balance of appetite-controlling neuropeptides was disrupted. The hypothalamus was poised to consume as many calories as were available, with no sense of satisfaction.

These findings expand on recent research published by Devaskar and colleagues in the June issue of the journal Diabetes, which found that if small babies are placed on a diet of moderately regulated calories during infancy, their propensity to become obese decreases. Because this was an early animal study, the UCLA researchers do not recommend that mothers of low-birth-weight infants start restricting their children's nutrition and suggest they consult with a pediatrician regarding any feeding questions.

About 10 percent of babies in the United States are born "small" -- defined as less than the 10th percentile by weight for a given gestation period. Some organizations define low birth weight as less than 2,500 grams -- or 5 pounds, 5 ounces -- at term.

Low birth weight can be caused by malnutrition due to a mother's homelessness or hunger or her desire not to gain too much weight during pregnancy. Additional causes include illness or infection, a reduction in placental blood, smoking, or use of alcohol or drugs during pregnancy.

Growth restriction before birth may cause lasting changes in genes in certain insulin-sensitive organs like the pancreas, liver and skeletal muscle. Before birth, these changes may help the malnourished fetus use all available nutrients. After birth, however, these changes may contribute to health problems such as obesity and diabetes.

Devaskar said the next phase of research will look at an intervention to reverse the hypothalamic neuropeptide changes that cause the central control of appetite to be set too high.

The study was funded by the National Institutes of Health.

In addition to Devaskar, the study was conducted by a team of UCLA researchers that included Bo-Chul Shin, Yun Dai, Manikkavasagar Thamotharan and L. Caroline Gibson.

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Less sleep, disrupted internal 24-hour clock means higher risk of diabetes and obesity

ScienceDaily (Apr. 11, 2012) — A study by researchers at Brigham and Women's Hospital (BWH) reinforces the finding that too little sleep or sleep patterns that are inconsistent with our body's "internal biological clock" may lead to increased risk of diabetes and obesity. This finding has been seen in short-term lab studies and when observing human subjects via epidemiological studies. However, unlike epidemiological studies, this new study provides support by examining humans in a controlled lab environment over a prolonged period, and altering the timing of sleep, mimicking shift work or recurrent jet lag.

See Also:Health & MedicineSleep Disorder ResearchInsomnia ResearchDiabetesMind & BrainSleep DisordersInsomniaObstructive Sleep ApneaReferenceCircadian rhythm sleep disorderJet lagCircadian rhythmSleep deprivation

The study will be electronically published on April 11, 2012 in Science Translational Medicine.

Researchers hosted 21 healthy participants in a completely controlled environment for nearly six weeks. The researchers controlled how many hours of sleep participants got, as well as when they slept, and other factors such as activities and diet. Participants started with getting optimal sleep (approximately 10 hours per night). This was followed by three weeks of 5.6 hours of sleep per 24-hour period and with sleep occurring at all times of day and night, thereby simulating the schedule of rotating shift workers. Thus, during this period, there were many days when participants were trying to sleep at unusual times within their internal circadian cycle-the body's "internal biological clock" that regulates sleep-wake and many other processes within our bodies. The study closed with the participants having nine nights of recovery sleep at the usual time.

The researchers saw that prolonged sleep restriction with simultaneous circadian disruption decreased the participants' resting metabolic rate. Moreover, during this period, glucose concentrations in the blood increased after meals, because of poor insulin secretion by the pancreas.

According to the researchers, a decreased resting metabolic rate could translate into a yearly weight gain of over 10 pounds if diet and activity are unchanged. Increased glucose concentration and poor insulin secretion could lead to an increased risk for diabetes.

"We think these results support the findings from studies showing that, in people with a pre-diabetic condition, shift workers who stay awake at night are much more likely to progress to full-on diabetes than day workers," said Orfeu M. Buxton, PhD, BWH neuroscientist and lead study author. "Since night workers often have a hard time sleeping during the day, they can face both circadian disruption working at night and insufficient sleep during the day. The evidence is clear that getting enough sleep is important for health, and that sleep should be at night for best effect."

This research was supported by the National Institute on Aging; National Heart, Lung and Blood Institute; National Center for Research Resources; Center for Clinical Investigation of the Harvard Clinical and Translational Science Center; Joslin Diabetes and Endocrinology Research Center Service Specialized Assay Core; the National Space Biomedical Research Institute; and Natural Sciences and Engineering Research Council of Canada.

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