Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 diabetes.
Alpha lipoic acid is an antioxidant that helps turn glucose into fuel for the body. It effectively improves insulin sensitivity and reduces symptoms of diabetic neuropathy, such as weakness, pain and numbness that’s caused by nerve damage. Although we make alpha lipoic acid and it can be found in some food sources, like broccoli, spinach and tomatoes, taking an ALA supplement will increase the amount that circulates in your body, which can be extremely beneficial when trying to reverse diabetes naturally. (17)
After two months under the care of the naturopath, John returned to his primary care doctor to discover that his hemoglobin A1c had dropped from 8.9% to 4.9%—a nondiabetic range. For eight months and counting, he’s been off all his diabetes medication. His last A1c reading was 5.1%. With the help of his naturopath, John seems to have reversed his diabetes.
Greek clover is an annual herb with aromatic seeds having medicinal properties. It is also known as fenugreek, and is largely used in curry. Greek clover has properties to lower down the levels of glucose in the body, which, in turn, controls diabetes. Also, when given in changeable doses of 25 gm to 100 gm on a daily basis, it was found to diminish reactive hyperglycemia in diabetic patients. Furthermore, levels of glucose, serum cholesterol, and triglycerides were also appreciably reduced. Alternatively, one can just stir two teaspoons of Greek clover seeds in powder form in warm milk and consume on a regular basis; it will control the levels of blood sugar and keep diabetes at bay. In case one does not want to have the powder in milk, seeds can be eaten wholly, too.
And when I talk about reducing certain carbohydrates, I mainly mean reducing your intake of refined carbohydrates such as pasta, rice and bread. Non starchy vegetables (such as broccoli, cabbage and cauliflower) are fine and can be eaten in abundance. Many fruits are packed with carbohydrates, so if you’re trying to reduce your carb intake, try and limit your intake to low-carb fruit, such as rhubarb, watermelon, berries, peaches and blackberries.
Cinnamon’s effectiveness as a treatment for diabetes has not been established. A prescription drug as ineffective as cinnamon likely wouldn’t pass FDA muster. Existing drug treatments for diabetes, on the other hand, are cheap, effective, and generally well tolerated. Compared to drug therapy, we don’t know if cinnamon can reduce the risk of mortality due to diabetes, or the progression to any of the other serious outcomes of diabetes. For my patients that insist on trying cinnamon, I’d caution them of the risks, and reinforce that cinnamon is no alternative for lifestyle changes and medication if necessary. It may be natural, sure, but that doesn’t mean it’s either safe or effective.
I feel the information is partial and not based scientific research, it treats values but what is the root of insulin resistance is avoided, the theory that taking the sugar and carbohydrates and enter protein and oil will improve the situation is based on clear results of the diet in shorten period, of course that the problem root is not treated and became worst, the insulin resistance is not a genetic only or abnormal function developed by the consume of carbs, evidence shows more and more that actually refined carbs and oil and animal protein is connected. I think modestly that the for those that want to reverse the chronic disease the best way is to test what is offered and then go to a fasting-sugar-overload test and see if the resistance has been removed, I will like to read if this has been checked by the doctors, thanks
Diabetes is a group of diseases characterized by elevated blood glucose levels due to defects in insulin secretion, insulin action, or both. According to the American Diabetes Association (ADA), type 2 diabetes usually begins with insulin resistance. For those people whose bodies resist insulin, the pancreas secretes extra insulin to maintain normal glucose levels. As the condition progresses, insulin production gradually decreases and eventually reaches a level of deficiency that can no longer maintain blood glucose in the normal range. But how type 2 diabetes presents and progresses can vary considerably, as noted by the ADA, and methods of treatment can vary from patient to patient.
According to studies, cinnamon may have a positive effect on the glycemic control and the lipid profile in patients with diabetes mellitus type 2. This is because it contains 18% polyphenol content in dry weight. This popular Indian spice can improve insulin sensitivity and blood glucose control. According to a study published in Journal Of The American Board Of Family Medicine, “cinnamon lowered HbA1C by 0.83% compared with standard medication alone lowering HbA1C 0.37%. Taking cinnamon could be useful for lowering serum HbA1C in type 2 diabetics with HbA1C >7.0 in addition to usual care.”
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Robert Ferry Jr., MD, is a U.S. board-certified Pediatric Endocrinologist. After taking his baccalaureate degree from Yale College, receiving his doctoral degree and residency training in pediatrics at University of Texas Health Science Center at San Antonio (UTHSCSA), he completed fellowship training in pediatric endocrinology at The Children's Hospital of Philadelphia.