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[BREAKTHROUGH] The Special Nutrient That Opens Your Fat Cells and DUMPS Your Stored Fat

New research published in the journal Nature, shows a potential breakthrough in the way your body handles different types of fat - especially omega-3 fatty acids.

What you eat, how much activity you get, and if you are including fruits, vegetables, and essential fats are all factors for helping you lose weight..

Now, however, researchers have shown that a receptor site located on your fat cells could play a key role in weight loss, fat accumulation (in your liver, arteries, and muscles), and specific characteristics reserved for people with diabetes.

Let me explain…

GRP120

GRP120 is a receptor site commonly found on the surface of your liver, fat, and muscle cells.

The function of the GRP120 receptor plays an important and functional role in the regulation of fat cells and your body’s ability to use unsaturated fatty acids - especially omega-3 fatty acids.

When unsaturated fatty acids bind to GRP120, they start a chain reaction, that research suggests, could lead to adipogenesis (the shift from adipocytes to adipose tissue), regulation of appetite, and your food choices.

The Research

Clinical research on mice deficient in the GRP120 gene that were fed a high-fat diet, showed increased obesity levels, glucose intolerance, and higher fat accumulation in the liver (fatty liver disease).

Also noted, these same mice showed a decrease in adipocyte differentiation, lipogenesis, and more hepatic (liver) lipogenesis.

The mice were unable to make more fat cells (adipocyte differentiation), which could take on more fat from the food they ate.  Instead, the fat was transferred to other areas of the body.

Lipogenesis, simply put, is the process of developing fat.  This is how your body converts fat found in food particles and stores it as body fat.

The mice deficient in GRP120 showed a reduction in fat being stored as body fat, but showed increased storage of fat in the liver and other organs.

The researchers also noted that GRP120-deficient mice showed signs of insulin resistance.

This resulted in a decrease in insulin signaling and higher inflammation levels (chronic and not acute) found in their fat cells.

Research suggests that when your fat cells are unable to utilize and store fat, the fat is then transferred and stored in other areas of your body, like your liver, muscles, and the walls of your arteries.

However, they also noted many similarities in regards to human subjects.

In people, increased fat in the liver, muscles, and walls of your arteries in combination with increased insulin resistance, could increase your risk for developing diabetes and heart disease.

The researchers noted that overweight or obese subjects showed higher levels of GRP120.

However, they did see a mutation in the GRP120 gene in overweight or obese subjects, which inhibited the activation of the gene to bind to unsaturated fatty acids.

This could decrease the activation of GRP120, which could increase obesity levels and increase their risk for diabetes and heart disease.

They concluded that GRP120 plays a significant role on sensing dietary fat, therefore disrupting the control of energy balance in both animal and human studies.

GRP120 and Your Health

Western diets, for the most part, are characterized by refined white flour, white sugar, and trans fats.

This could increase your omega-6 to omega-3 ratio, which research suggests, has the ability to increase chronic inflammation levels.

Chronic inflammation could target your fat cells, potentially deactivating the GRP120 receptor located on your fat, liver, or, muscle cells.

The GRP120 receptor is activated in the presence of omega-3 fatty acids, and when activated, has the potential to reduce chronic inflammation, create new fat cells, utilize more fat for energy, reduce inflammation, and lower fat stored in other organs like the liver and arteries.

This could stimulate weight loss and, as research suggests, lower your risk for heart disease and diabetes.

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References:

Ichimura, A.  Hirasawa, A.  Poulain-Godefroy, O.  Bonnefond, A.  Hara, T.  Yengo, L.  Kimura, I.  Leloire, A.  Liu, N. Lida, K.  Choquet, H.  Besnard, P.  Lecoeur, C.  Vivequin, S.  Ayukawa, K.  takeuchi, M.  Ozawa, K.  Tauber, M.  Maffeis, C.  Morandi, A.  Buzzetti, R.  Elliot, P.  Pouta, A.  Jarvelin, MR.  Korner, A.  Kiess, W.  Pigeyre, M.  Caiazzo, R.  Hul, WV.  Gaal, LV.  Horber, F.  Balkau, B.  Levy-Marchal, C.  Rouskas, K.  Kouvatsi, A.  Hebebrand, J.  Hinney, A.  Scherag, A.  Pattou, F.  Meyre, D.  Koshimizu, T.  Wolowczuk, I.  Tsujimoto, G.  Froguel, P.  Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human.  Nature.  2012.  doi: 10.1038/nature10798.