A new genomic study has discovered a link between metabolic diseases, digestion of milk, and microRNA. The research was a collaboration of a dozen American and European institutions led by the University of California Berkley.
The paper was recently published in the journal Cell describing microRNA, or non-coding RNA that do not produce proteins, and their role in metabolic conditions such as diabetes, celiac disease, and lactose intolerance.
Historically, the human body stopped producing lactase, the enzyme that enables the digestion of milk sugar called lactose, after infancy. Then, a few thousand years ago, a lactase gene appeared in Europeans, allowing adults to digest milk. Adult milk consumption throughout Europe helped people survive off of their livestock when food resources were scarce.
Metabolic Diseases and Lactose Intolerance
Today, there are numerous metabolic diseases due to carbohydrate-rich diets, processed foods, and sedentary lifestyles. Excess food consumption has resulted in conditions such as insulin resistance and high blood pressure, increasing the rates of cancer, diabetes, heart disease, and stroke.
For years, obesity has become an increasing global problem as scientists have searched for genetic factors that contribute to obesity. However, researchers have not been able to found a single "obesity gene" yet.
What the researchers found in the new study is a specific chromosomal region, called a locus, linked to lactase, obesity, and type 2 diabetes. Within the chromosome, the locus was also a microRNA called miR-128-1 which helps regulate cholesterol levels.
Professor Anders Näär from UC Berkeley said that discovering both lactase and miR-128-1 in the same region meant "there might be a connection of the microRNA to the human evolutionary adaptation to famine." This is the first time that microRNA has been associated with molecular functions outside their roles in tissues and cells such as regulating metabolism.
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MicroRNA Affecting Metabolism
Using mice models, the researchers either genetically deleted the miR-128-1 function or used therapeutic molecules. Those with the specific microRNA region turned off had faster metabolism, stored less fat, and did not have insulin resistance. The results suggest that miR-128-1 may play an essential role in metabolism by increasing energy storage through accumulated fat.
Näär described miR-128-1 "as a master regulator of the energy storage programs in many metabolically active organs that may contribute to metabolic diseases such as obesity and type 2 diabetes linked to nutritional overabundance, as well as genetic selection in humans for obesity and type 2 diabetes. It may also be a potential target for therapies associated with treating metabolic disorders. Drugs that treat metabolic disorders typically focus on genes and proteins, not non-coding microRNA.
The study also "brings together ancient evolutionary traits that date back to human domestication of animals and adapting to milk products, together with the current epidemic of obesity and metabolic dysregulation that contribute to both heart disease and cancer risk," said Daniel Haber from the Mass General Cancer Center. It turns out that metabolic diseases and associated illnesses are not caused by "real gene, but rather a small piece of regulatory RNA that controls how groups of genes are coordinated."
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