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Leptin May Benefit Diabetics

02/01/10

LeptiFitâ„¢New research published in the January issue of Cell Metabolism has found that the hormone leptin helps to correct diabetes in animal models and perhaps in human subjects as well.1

Leptin is a hormone produced by adipocytes (fat cells) that regulates body fat storage by modulating satiety, glycemic control and metabolism. Leptin triggers the sensation of satiety, giving the feeling of having eaten "enough".

Generally speaking when a person is properly nourished, serum leptin levels increase, and hunger levels decrease. Additionally, leptin plays a role in metabolic regulation and helps the body utilize stored fat. Problems arise, however, when people experience leptin resistance, a condition which binds leptin and reduces the amount of leptin in the blood.

As researchers are rapidly discovering, weight management is not the sole function of leptin. In the January newsletter we featured research that found that Leptin may reduce the risk of Alzheimer's Disease by as much as 19%.2

Weight loss alone can improve diabetes, leaving previous results unclear if leptin improved diabetes due to the weight loss it caused, or if there was another mechanism in play. This new study's design confirmed the latter; leptin's anti-diabetic effect is independent of its ability to cause weight loss.

Diabetes is a disease in which the body does not produce or use insulin properly. Insulin is responsible for converting sugars, starches and other carbohydrates into energy for the body.

To determine how leptin improved diabetes, the researchers first conducted studies on mice to determine lowest level of leptin that could be administered that would reverse insulin resistance and diabetes without also causing the mice to lose weight or reduce their appetites. The levels turned out to be surprisingly low. The researchers found that 12.5 nanograms per hour significantly reduced blood glucose levels while twice that, 25 nanograms per hour completely normalized blood glucose and insulin levels without causing weight loss.

As it turns out, leptin triggers a gene in the liver to produce a protein called "Insulin-like Growth Factor Binding Protein 2" or IGFBP2 for short. IGFBP2 helps the body regulate glucose levels through a rather complex process that involves IGFBP2 binding to the IGF-1 and IGF-2 receptor sites, which in turn decreases insulin resistance.

After demonstrating that leptin activated the IGFBP2 gene and IGFBP2 production, the researchers focused their study on the effects of increasing IGFBP2 expression. Increasing the IGFBP2 expression in obese and diabetic mice reversed diabetes in the animals. The treated mice had 3 times the response to insulin than the untreated mice.

Looking at humans, the researchers confirmed that humans with diabetes also have low levels of IGFBP2. As with mice, those low levels of IGFBP2 can be increased with low doses of leptin.

In conclusion the researchers stated that "we have developed a set of conditions in which leptin treatment potently improves diabetes independent of its ability to correct weight and food intake. This protocol was used to identify IGFBP2 as a leptin-regulated gene whose expression is correlated with leptin's anti-diabetic effect."

Clinical studies will have to be conducted before there is a full understanding of the impact of leptin on diabetes. However, this appears to be a major breakthrough in the understanding of both leptin's roles in the body and how it may regulate blood sugar.

Our LeptiFit™ Leptin Enhancing Formula works by reducing leptin resistance, and therefore  increasing the amount of free leptin in the blood. Higher levels of leptin allow leptin to reach the brain and perform its multitude of tasks, not the least of which is to curb appetite.

Learn more about our LeptiFit™ Leptin Enhancing Formula here.


 

1. Hedbacker, K., K. Birsoy, et al. "Antidiabetic effects of IGFBP2, a leptin-regulated gene." Cell Metab 11(1): 11-22.

2. Lieb, W., A. S. Beiser, et al. (2009). "Association of plasma leptin levels with incident Alzheimer disease and MRI measures of brain aging." Jama 302(23): 2565-72.





 

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