One Single Enzyme May be the Key to the Development of DiabetesAugust 18, 2014
One Single Enzyme May be the Key to the Development of Diabetes
Reference: August 14th
issue of Molecular and Cellular Biology
There may just one enzyme the gets us in trouble when we get overweight. About 40% of Americans are currently in that state of diabetes or prediabetes, and that’s if you count a blood sugar over 100. I believe the Whitehall Study shows us that a blood glucose over 86, two hours after a meal is what really matters, as every point over 86 means your risk of developing diabetes increases by 5%. So, 100 and 126 are just arbitrary numbers that we have picked for levels of increasing risk. If we take the Whitehall study, my experience (there is no data) is that closer to 90% of us are “not perfect”.
Developing Type II diabetes means you have insulin around, but you are insulin resistant and your fat cells just can’t respond to insulin. If you measure insulin levels routinely, you see folks who have normal blood sugars, but very high insulin levels – and they are universally overweight. Obesity makes for larger fat cells that aren’t able to respond to the insulin signal to take up glucose or fat, so your glucose and your fat levels in your blood increase.
What’s the critical enzyme from this study? One called 12-Lipooxygenase, or 12-LO. It is present ONLY when people become overweight. 12-LO manufactures small molecules called HETEs
(hydroxyeicosatetraenoic acid) which damage the mitochondria in the pancreas cell. The mitochondria
are the power plants that produce energy for the cell. With damaged mitochondria, the cells can’t produce enough insulin to keep up with the demand caused by insulin resistance promoted by obesity.
The researchers genetically engineered the mice to have no 12-LO enzyme at all in their pancreas glands, then fed them high fat diets versus low fat diets. The researchers fed both control and knockout mice the Western Diet – high in saturated fat – and both sets got obese. And insulin resistant. Then, they looked at their pancreas glands. The Knockout mice with no 12-LO still had intact and undamaged pancreas glands whereas the control mice had damaged pancreas glands. This implicates 12-LO as the missing ingredient of causing damage that then leads to pancreas failure and overt diabetes. 12-LO may be the cause of pancreatic failure that ensues when we become obese and our blood sugar starts climbing and we become insulin resistant.
What the authors don’t address or explain is that a high fat diet causes obesity mostly when it’s combined with refined sugars and carbohydrates. That’s the real problem with the “Western Diet”. Fat does not cause the release of insulin, whereas carbohydrates do. To remain trim and fit, and not develop diabetes one needs to eat fat. (Please read the book The Big Fat Surprise
by Nina Teicholz).
WWW. What Will Work for Me. I’m not sure I completely agree with the explanations this author provides about diabetes, but I love the discovery of a single specific enzyme that causes damage to the pancreas gland and causes it to finally poop out. We can’t let low grade sugar persist without eventually running the gauntlet of overt diabetes.
- 12-LO in present in pancreas cells only when we become obese. T or F
- 12-LO makes damaging molecules that injure our pancreas glands by damaging their mitochondria, which leads to “power failure” and the inability to make sufficient insulin to meet demand. T or F
- About 40% of American’s have prediabetes or diabetes. T or F
True if you use the measurement of 100 for glucose, but many more if you use the Whitehall data to support 86 as the normal level
- I can lower my risk for diabetes by losing weight. T or F
- So, I can get rid of 12-LO by losing weight