Obesity is no longer a problem of appearance. At present, more and more diseases have been proved to be closely related to obesity, which has attracted more and more scientists to devote themselves to research in this field. Recently published Science and Nature two top magazines published new achievements in this field. Researchers from Yale University in the United States and Carleton University in Canada have discovered the molecular link between nicotine and weight loss, and explain why smokers are on average thinner than non-smokers, and why people around the world report that They will use smoking as a method of weight control. Smoking is still the leading cause of preventable death in developed countries. Understanding its related molecular mechanisms can help develop nicotine-based treatments to help people quit smoking and control obesity and metabolic diseases. In this article, the researchers found that nicotine reduces a person ’s appetite by activating a specific set of neurons in the brain. They conducted a set of molecular, pharmacological, electrophysiological, behavioral and gene knockout experiments. Nicotine affects a series of central nervous system circuits (called the hypothalamic melanocortin system) by activating certain receptors. The researchers believe that these receptors in turn increase the activity of POMC neurons (these neurons are known to have an effect on obesity in humans and animals) and the activity of a specific set of melanocortin-4 receptors. This result is helpful in explaining the molecular and synaptic mechanisms associated with nicotine-related weight and appetite reduction. Researchers from Switzerland found that the up-regulated expression of two microRNA molecules may be the key to the dysfunction of insulin signaling that can lead to obesity and type 2 diabetes. Scientists at the Swiss Federal Institute of Technology (ETH Zurich) have found that silencing these two microRNAs improves glucose sensitivity in obese mice. The research paper "MicroRNA 103 and 107 Regulates Insulin Sensitivity" was published in Nature on June 8, 2011. This finding may point the way to potential obesity treatment in humans.
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MicroRNA, a small part of non-coding RNA, shuts down the complete gene expression network by combining and silencing protein synthesis template mRNA. Several studies have shown that microRNA is involved in cancer, diabetes, heart disease and neurological disorders. A microRNA sequence under study is being clinically tested in humans as a potential treatment for hepatitis C.
Markus Stoffel, a molecular physiologist at the Swiss Federal Institute of Technology, has long wanted to see if certain microRNAs are associated with obesity and diabetes. To this end, he and his colleagues performed gene expression analysis and found that both microRNAs 103 and 107 were up-regulated in mice and humans with fatty liver disease, which is a precursor to insulin resistance and diabetes.
To confirm that these two microRNAs cause insulin resistance, Stoffel and his colleagues used a viral vector to express these two microRNAs in healthy mice, and as a result they quickly developed hyperglycemic symptoms. Then they selected two groups of obese mice-one group became genetically modified to gain weight, while the other group consisted of normal mice, became fat by feeding high-fat foods, and silenced these two microRNAs in these two groups of mice. Expression, the results showed that glucose metabolism in liver cells and fat cells of these two groups of mice was improved.
The researchers then determined through gene expression experiments that these two microRNAs reduce insulin sensitivity by turning off the expression of a membrane protein called caveolin-1. In adipocytes, caveolin-1 can stabilize the insulin receptor.
Two top publications published articles focusing on the mystery of weight