Many who struggle with their weight will often blame a “slow” metabolism – meaning their bodies do not burn calories as quickly or as efficiently as others’.
For those who do suffer this condition, investigators from Beth Israel Deaconess Medical Center (BIDMC) say they have found a genetic “switch” that can accelerate a person’s basal metabolic rate – leading to a dramatic reduction in the risk for obesity and diabetes.
Their research, published in the journal Nature, involves turning off a gene that encodes a protein called nicotinamide N-methyltransferase (NNMT), which is found in the fat cells and the liver. NNMT is known to process vitamin B3 and has been previously linked with certain types of cancers.
In order to lower the expression of the NNMT gene, the researchers used antisense oligonucleotide (ASO) technology, which allowed them to interfere with the expression of the gene only in the fat cells and the liver. ASOs are short molecular strings of DNA, which can be designed to prevent the synthesis of specific proteins.
When the researchers turned off the NNMT gene in mice on high-fat diets, the mice did not gain as much weight compared to when the NNMT gene was functioning normally. Furthermore, the mice did not change their eating or exercise habits, meaning the NNMT solely affected the mice’s basal metabolic rates.
More than 1/3 of adults in the United States are considered obese, and 25.8 million people – 8.3 percent of the American population – have diabetes, according to the Centers for Disease Control and Prevention.
Nature - Metabolism: Targeting a fat-accumulation gene An enzyme that links two metabolic hubs has been found to be upregulated in the fat cells of overweight mice. Inhibition of the gene encoding this enzyme protects mice from diet-induced obesity.
Nature - Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity
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For those who do suffer this condition, investigators from Beth Israel Deaconess Medical Center (BIDMC) say they have found a genetic “switch” that can accelerate a person’s basal metabolic rate – leading to a dramatic reduction in the risk for obesity and diabetes.
Their research, published in the journal Nature, involves turning off a gene that encodes a protein called nicotinamide N-methyltransferase (NNMT), which is found in the fat cells and the liver. NNMT is known to process vitamin B3 and has been previously linked with certain types of cancers.
In order to lower the expression of the NNMT gene, the researchers used antisense oligonucleotide (ASO) technology, which allowed them to interfere with the expression of the gene only in the fat cells and the liver. ASOs are short molecular strings of DNA, which can be designed to prevent the synthesis of specific proteins.
When the researchers turned off the NNMT gene in mice on high-fat diets, the mice did not gain as much weight compared to when the NNMT gene was functioning normally. Furthermore, the mice did not change their eating or exercise habits, meaning the NNMT solely affected the mice’s basal metabolic rates.
More than 1/3 of adults in the United States are considered obese, and 25.8 million people – 8.3 percent of the American population – have diabetes, according to the Centers for Disease Control and Prevention.
Nature - Metabolism: Targeting a fat-accumulation gene An enzyme that links two metabolic hubs has been found to be upregulated in the fat cells of overweight mice. Inhibition of the gene encoding this enzyme protects mice from diet-induced obesity.
Nature - Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity
Read more »
