14 DAY TRIAL // In order to get slim, you are trying hard to reduce the fat input in your alimentation.
But in fact, most fat from your body comes from sugars.
More precisely, sweets and starches (from bakery products, rice, potatoes), which provide the organism huge amounts of glucose.
A new study shows how glucose is linked to fats metabolism, activating the Liver X Receptors (LXR) a and b. The LXRs was known to react to nutrients like oxysterols (short-lived derivatives of cholesterol) and tuning gene expression linked to cholesterol and fat metabolism. "When you eat, glucose pours into the gut and is recognized by LXR in the liver, which then activates expression of the enzymes that turn excess glucose into triglycerides that are stored as fat," said Enrique Saez, a Scripps Research scientist.
"The fact that our study demonstrates that LXR does both-it binds to glucose and it induces fatty acid synthesis-is significant and makes LXR a potential target for diabetes and obesity treatments."
"In some recent animal studies activation of LXRs using synthetic molecules also induced regression of atherosclerosis, the clogging, narrowing, and hardening of the body's large arteries and blood vessels that can lead to stroke, heart attack, and eye and kidney problems. Elevated levels of pathogenic cholesterols, also known to bind LXR, are a primary risk for development of atherosclerosis." added Saez.
"The integration of glucose sensing and control of lipogenesis (fat synthesis) by LXR may explain why low-fat/high-carbohydrate diets induce hypertriglyceridemia (an elevated level of triglycerides in the blood)," Saez said.
In other words, you can have a low-fat diet, but if it is reach in sugars, you get fat. "LXR an sense surplus glucose, induce fatty acid synthesis, and prompt the liver's export of triglycerides into the bloodstream. Since LXR acts as the body's sensor of a buildup of pathogenic cholesterol, its ability to bind both glucose and oxysterols suggests that LXR may be a link between hyperglycemia and atherosclerosis."
The study was initiated to investigate LXR as a drug target for atherosclerosis. But synthetic LXR in mice made them more efficient in metabolizing glucose and LXR suppressed new production of glucose in the liver. In fact, glucose bound directly to LXR.
That was a surprise, because glucose is not a typical ligand that activates nuclear receptors, transcription factors that coordinate gene expression in response to hormonal and environmental signals. "This discovery represents the first signaling pathway where a carbohydrate activates a nuclear receptor, although the precise mode of binding remains unknown." said Saez.
Then mice were put on exclusive sucrose or D-glucose diets, devoid of cholesterol to minimize naturally occurring oxysterols. D-glucose and GW3965 (a synthetic LXR activator) induced the same changes in the hepatic gene expression, thus LXR is sensitive to glucose, responding to increasing liver glucose uptake. This LXRs sensitivity to glucose and its derivatives is very specific: no effect was seen in other nuclear receptors tested. "New studies will focus on the question of whether glucose levels in other tissue types, such as the pancreas, activate LXR," Saez added.