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Omega-3's POWERFUL Role In Insulin Resistance

By Kevin DiDonato MS, CES


Adiponectin is a powerful hormone secreted by your fat cells or your white adipose tissue.

And research suggests that Adiponectin stimulates the oxidation of fatty acids, can suppress gluconeogenesis (the production of new glucose), and it could stop macrophage from transforming.

Being overweight or obese could lower the production and secretion of Adiponectin from your fat cells.

However, the latest research shows that omega-3 fatty acids could potentially increase Adiponectin levels and reduce markers associated with insulin resistance.

Let me explain…

Insulin Resistance

Insulin resistance refers to a state in your body, when your cells are unable to use insulin to shuttle sugar from your blood into your cells.

This results in an increase in the amount of sugar in your blood.

Insulin resistance could affect both your liver and fat cells.

If insulin resistance affects your liver, research suggests that your liver reduces glucose synthesis and the storage of glucose.

This could cause your liver to be unable to suppress glucose production and it being released into your bloodstream.

If insulin resistance affects your fat cells, it could result in a decreased uptake of fatty acids.

According to research, this could prevent fat cells from taking on more fatty acids and storing them for later use.

This could also lead to an increased breakdown of fatty acids in your fat cells which could increase the amount of fatty acids in your bloodstream.

And, according to some studies, this could increase your risk for developing heart disease.

Plus, increased levels of insulin and blood sugar could significantly raise your risk for metabolic syndrome.

Markers for Insulin Resistance

Being overweight or obese could lead to your body producing blood markers for insulin resistance.

These markers could be pro-inflammatory in nature, or could lead to other conditions.

Markers, such as Resistin and RBP-4, could increase inflammation and increase the risk for atherosclerosis, according to some research.

Resistin is produced by monocyte cells and activated by macrophages in your body.

However, when there is an overproduction of Resistin and RBP-4, this could encourage insulin resistance in your body.

An overexpression of these Resistin, in particular, could decrease your liver’s ability to stop glucose production and them from being released into your bloodstream, and the ability of your muscles to take in glucose.

Omega-3, Oral high-fat diet, and Insulin Resistance

Researchers aimed to see if omega-3 fatty acids had the ability to reduce markers associated with insulin resistance, especially after a being fed a high-fat diet.

They recruited 167 participants (82 males and 85 females).

They were administered either 1 gram (1000 mg) of omega-3 fatty acids or a placebo, three times a day with meals for six months.

They concluded that the omega-3 fatty acid group showed greater improvements in cholesterol profiles and increased adiponectin levels compared to the control group.

Also noted, the omega-3 group showed an improvement in markers associated with insulin resistance after ingesting a high-fat diet.

New Role of Omega-3 Fatty Acids

Insulin resistance is a condition which could potentially lead to metabolic syndrome or even diabetes, if left untreated.

This could also increase your risk for heart disease or other chronic diseases and conditions.

According to research, omega-3 fatty acids could have the ability to lower cholesterol, improve heart health, improve cognitive function and depression, and reduce markers associated with insulin resistance.

Including omega-3 fatty acids into your daily diet plan, could improve your health and well-being, research suggests.


NEXT: Find Out More Powerful Benefits Of Omega-3 Fatty Acids >>

Discover What Your Doctor NEVER Wants You To Know About Fish Oil >>

 

 





Resources:

Derosa, G.  Cicero, A.  Fogan, E.  D’Angelo, A.  Bonventura, A.  Maffoilo, P.  Effects of n-3 PUFA on insulin resistance after an oral fat load.  Eur J Lipid Sci Techno.  2011. Vol. 113(8):pp. 950-960.