Obesity, defined as a body mass index (BMI) of 30 kg/m2 or more, is common in many parts of the world. Obesity rates are alarmingly high; many populations continue to see steady increases in obesity; and there are striking, persistent racial and ethnic disparities.
The balance between calorie intake and energy expenditure determines a person’s weight. If a person eats more calories than he or she burns, the person gains weight. The most common causes of obesity are overeating and physical inactivity.
Now, scientists have discovered hormonal links between diet and obesity, suggesting low levels of a circulating hormone called adropin predict increased weight gain and metabolic dysregulation during consumption of a high-sugar diet in a nonhuman primate model.
Scientists have previously determined that peptide hormone adropin regulates whether the body burns glucose or fat. The levels of hormone may contribute to diabetes and the associated reduced ability of the body to use glucose. The high adropin levels lead to lower BMI levels.
In the current study, scientists explored adropin’s role in metabolic health. They examined the plasma of 59 adult male rhesus macaques fed a high sugar diet.
Overall, consumption of the fructose diet produced a 10% gain in body weight and increases of fasting levels of insulin, indicating insulin resistance, which reduces glucose use and elevated fasting triglycerides which in humans increases the risk of cardiovascular disease.
Animals with low plasma adropin concentrations developed more severe metabolic syndrome. Interestingly, the development of type 2 diabetes was only observed in animals with low plasma adropin concentrations. These animals also showed more pronounced dysregulation of glucose and lipid metabolism.
Fasting hyperglycemia was also limited to animals with low circulating adropin, indicating glucose intolerance.
Scientists also examined a baboon transcriptome (genetic) data set to explore the expression of the adropin gene in a nonhuman primate. Adropin is encoded by the Energy Homeostasis Associated (ENHO) gene.
Andrew Butler, Ph.D., professor of pharmacology and physiology at SLU said, “Monkeys with low adropin may therefore not be oxidizing glucose as well, explaining their higher fat content as the glucose is converted to lipids instead of being used as a metabolic fuel.”
“What we show in this paper is that expression of the ENHO gene is higher in the daytime and lower at night in most primate tissues.”
“This is consistent with the idea that adropin expression is controlled via “clock-related” mechanisms.”
Every cell in the body maintains its own internal clock to control daily rhythms in metabolism. There is a growing awareness of the importance of the biological clocks that control the “circadian rhythm” in health and disease. The current finding suggests that adropin may link the biological clock to rhythms in the way the body uses sugar and fats as metabolic fuel.
Butler said, “To further get at what this might mean, data suggest that enhanced use of glucose as fuel happens at certain times of the day. At night time, the body relies on energy reserves stored as lipids in fat cells and in the daytime relies more on the carbohydrates coming in from the diet.”
“In this way, stimulation of adropin expression by our internal clocks may contribute to increasing the use of glucose as a metabolic fuel during the daytime.”
“Other findings show that adropin expression is co-regulated with clusters of genes involved in glucose and fat metabolism in the liver.”
The study is published in the Journal of Biological Chemistry.