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.
Curcumin is a bright yellow chemical produced by the spice turmeric, among other plants. Curcumin seems to have multiple benefits for diabetes symptoms. It has been shown to be a marked inhibitor of reactive oxygen species that promote oxidation damage in cells. Curcumin lowers inflammatory chemicals like tumor necrosis factor-alpha, and that’s good because TNF-a causes insulin resistance and irritates fatty livers. Curcumin can reduce another pro-inflammatory chemical called NF-KB. The above-mentioned actions provide a benefit in diabetes protection and reduce the risk of developing diabetes symptoms and complications. Curcumin has also been shown to enhance pancreatic beta cell functioning and reduce fatty liver deposition. It reduces high blood sugar, A1C, and insulin resistance. It was also shown to reduce the onset of Alzheimer’s disease, and that is a higher risk in diabetic patients than in nondiabetic patients. A good dose is 200 to 3,000 mg a day.
The researchers have cured mice, which are genetically similar to people but different enough that new rounds of animal testing — and millions of dollars more — are needed before human trials can begin. The researchers’ approach is sure to garner skeptics, at least in part because it is a significant departure from the many other attempts at curing diabetes, which typically involve transplanting new cells and/or suppressing the immune system’s attempts to kill off useful ones.
Qi (pronounced “chi”) is translated into English as vital energy. It is defined in terms of function rather than as a discrete substance, and it is what animates us and allows us to move and maintain the activities of life. The origins of Qi include “congenital”’ (prenatal) Qi—that which is inherited from our parents—and “acquired” Qi—that which is incorporated from food and air.4
Whenever this seasonal fruit is available in the market, try to include it in your diet as it can be very effective for the pancreas. Else you can make a powder of dried seeds of Jambul fruit and eat this powder with water twice a day. This fruit is native to India and its neighboring countries but you can find it at Asian markets and herbal shops.

A new class of medications called DPP-4 inhibitors help improve A1C without causing hypoglycemia. They work by by preventing the breakdown of a naturally occurring compound in the body, GLP-1. GLP-1 reduces blood glucose levels in the body, but is broken down very quickly so it does not work well when injected as a drug itself. By interfering in the process that breaks down GLP-1, DPP-4 inhibitors allow it to remain active in the body longer, lowering blood glucose levels only when they are elevated. DPP-4 inhibitors do not tend to cause weight gain and tend to have a neutral or positive effect on cholesterol levels. Alogliptin (Nesina), linagliptin (Tradjenta), saxagliptin (Onglyza), and sitagliptin (Januvia) are the DPP-4 inhibitors currently on the market in the US.


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.
However, the observation that normalization of glucose in type 2 diabetes occurred within days after bariatric surgery, before substantial weight loss (15), led to the widespread belief that surgery itself brought about specific changes mediated through incretin hormone secretion (16,17). This reasoning overlooked the major change that follows bariatric surgery: an acute, profound decrease in calorie intake. Typically, those undergoing bariatric surgery have a mean body weight of ∼150 kg (15) and would therefore require a daily calorie intake of ∼13.4 MJ/day (3,200 kcal/day) for weight maintenance (18). This intake decreases precipitously at the time of surgery. The sudden reversal of traffic into fat stores brings about a profound change in intracellular concentration of fat metabolites. It is known that under hypocaloric conditions, fat is mobilized first from the liver and other ectopic sites rather than from visceral or subcutaneous fat stores (19). This process has been studied in detail during more moderate calorie restriction in type 2 diabetes over 8 weeks (20). Fasting plasma glucose was shown to be improved because of an 81% decrease in liver fat content and normalization of hepatic insulin sensitivity with no change in the insulin resistance of muscle.
Another factor to consider when determining when to take your diabetes medicines is how well you can follow the regimen your doctor recommends. For any drugs to be effective, you have to take them. Ideally, your medication schedule should be incorporated into your daily routine; only having to remember to take your diabetes pills once a day may make things easier for you. Not much evidence is available that taking saxagliptin and glipizide at different times will provide a better blood-glucose-lowering effect. The most important thing is to take them regularly and without missing any doses. In addition to taking the diabetes medicines you’ve been prescribed, other ways to help improve your blood glucose levels are to engage in healthy lifestyle habits, such as regular physical activity and a healthy diet.

Called ALA for short, this vitamin-like substance neutralizes many types of free radicals. A build-up of free radicals, caused in part by high blood sugar, can lead to nerve damage and other problems. ALA may also help muscle cells take up blood sugar. In a German study, a team of scientists had 40 adults take either an ALA supplement or a placebo. At the end of the four-week study, the ALA group had improved their insulin sensitivity 27 percent. The placebo group showed no improvement. Other studies have shown a decrease in nerve pain, numbness, and burning.
One can't, in spite of the initial reported success of following a 600 kcal vegetarian diet for 8 weeks cured all 11 participants of their diabetes, resulting in an enormous very beneficial weight loss of 15 kg and reversal of pancreatic fat infiltration that many think is the underlying defect causing type 2 diabetes, see this 2011 paper Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol only just 3 months afterwards diabetes had recurred in 5 out of the 11 see Diet reverses Type 2 Diabetes

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Within the hepatocyte, fatty acids can only be derived from de novo lipogenesis, uptake of nonesterified fatty acid and LDL, or lipolysis of intracellular triacylglycerol. The fatty acid pool may be oxidized for energy or may be combined with glycerol to form mono-, di-, and then triacylglycerols. It is possible that a lower ability to oxidize fat within the hepatocyte could be one of several susceptibility factors for the accumulation of liver fat (45). Excess diacylglycerol has a profound effect on activating protein kinase C epsilon type (PKCε), which inhibits the signaling pathway from the insulin receptor to insulin receptor substrate 1 (IRS-1), the first postreceptor step in intracellular insulin action (46). Thus, under circumstances of chronic energy excess, a raised level of intracellular diacylglycerol specifically prevents normal insulin action, and hepatic glucose production fails to be controlled (Fig. 4). High-fat feeding of rodents brings about raised levels of diacylglycerol, PKCε activation, and insulin resistance. However, if fatty acids are preferentially oxidized rather than esterified to diacylglycerol, then PKCε activation is prevented, and hepatic insulin sensitivity is maintained. The molecular specificity of this mechanism has been confirmed by use of antisense oligonucleotide to PKCε, which prevents hepatic insulin resistance despite raised diacylglycerol levels during high-fat feeding (47). In obese humans, intrahepatic diacylglycerol concentration has been shown to correlate with hepatic insulin sensitivity (48,49). Additionally, the presence of excess fatty acids promotes ceramide synthesis by esterification with sphingosine. Ceramides cause sequestration of Akt2 and activation of gluconeogenic enzymes (Fig. 4), although no relationship with in vivo insulin resistance could be demonstrated in humans (49). However, the described intracellular regulatory roles of diacylglycerol and ceramide are consistent with the in vivo observations of hepatic steatosis and control of hepatic glucose production (20,21).
Diabetes education is very important for any diabetic or a person who has a diabetic at home. The education helps an individual to know more about this dreadful disease. Once educated, the individual can control diabetes in a better manner. Administering insulin, medications, and understanding emergency situations like hypoglycemic attacks, etc. are major points of diabetes education. It also includes the diet a diabetic should avoid and have. Diabetes education is very essential for each and every diabetic and individual who has someone close living with diabetes.
You should have no more than three of these “feeding times” per day. The reason limiting the number and duration of your meal times is so important has to do with staying out of the vicious cycle of increasing insulin resistance. To get smart on insulin resistance — the cause of both type 2 diabetes and obesity — read Dr. Jason Fung’s book, The Obesity Code: Unlocking the Secrets of Weight Loss, or watch his free lecture on YouTube.
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