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.
The term diabetes includes several different metabolic disorders that all, if left untreated, result in abnormally high concentration of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.
Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.
So you go to your doctor. What does he do? Instead of getting rid of the toxic sugar load, he doubles the dose of the medication. If the luggage doesn’t close, the solution is to empty it out, not use more force to . The higher dose of medication helps, but only for a time. Blood sugars go down as you force your body to gag down even more sugar. But eventually, this dose fails as well. So then your doctor gives you a second medication, then a third one and then eventually insulin injections.

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
My Mother is suffering from type 1 diabetes since last 20yrs..she is using alopathy medicines but.. we are not able to control the sugar levels to normal. today only i gone thru this site..and got very usefull information on diabetes treatment natural way. its really a great effort ..i wish that every one get very usefull tips for their health problems..
So, can you “reverse” diabetes? No – but you can manage it very well with the help of a Certified Diabetes Educator (CDE) and a knowledgeable primary care physician or endocrinologist. There are even prescription apps available to bridge the care that your clinicians can give you between visits and apps that offer virtual CDE’s for greater assistance.
High blood glucose in diabetic people is a risk factor for developing gum and tooth problems, especially in post-puberty and aging individuals. Diabetic patients have greater chances of developing oral health problems such as tooth decay, salivary gland dysfunction, fungal infections, inflammatory skin disease, periodontal disease or taste impairment and thrush of the mouth.[57] The oral problems in persons suffering from diabetes can be prevented with a good control of the blood sugar levels, regular check-ups and a very good oral hygiene. By maintaining a good oral status, diabetic persons prevent losing their teeth as a result of various periodontal conditions.
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).
The researchers followed the participants after they had completed an eight-week low-calorie-milkshake diet and returned to normal eating. Six months later, those who had gone into remission immediately after the diet were still diabetes-free. Though most of those who reversed the disease had had it for less than four years, some had been diabetic for more than eight years.
Eating a balanced diet is vital for people who have diabetes, so work with your doctor or dietitian to set up a menu plan. If you have type 1 diabetes, the timing of your insulin dosage is determined by activity and diet. When you eat and how much you eat are just as important as what you eat. Usually, doctors recommend three small meals and three to four snacks every day to maintain the proper balance between sugar and insulin in the blood.
Any food that you ingest is processed and metabolized by the body. Food is broken down into the various building blocks the body needs, and what cannot be metabolized or used is processed and removed by the liver. Protein and fats are used for muscle and tissue regeneration and other processes in the body. Carbohydrates are typically a fast fuel for the body, but when more are eaten that the body immediately needs, they must be stored. A simple explanation from a previous post:
Most of those foods are refined, processed starches and sugars. Lots of diets place people on a restricted plan that doesn’t allow the refined, processed starches and sugars, and people lose weight, regain good BG control and feel better. However, in most cases, the weight comes back and weight creeps up and BG begins rising again due to the inability to sustain many of these diets.
Pancreatic islet transplantation is an experimental treatment for poorly controlled type 1 diabetes. Pancreatic islets are clusters of cells in the pancreas that make the hormone insulin. In type 1 diabetes, the body’s immune system attacks these cells. A pancreatic islet transplant replaces destroyed islets with new ones that make and release insulin. This procedure takes islets from the pancreas of an organ donor and transfers them to a person with type 1 diabetes. Because researchers are still studying pancreatic islet transplantation, the procedure is only available to people enrolled in research studies. Learn more about islet transplantation studies.
In fact, the CDC notes that losing just 5 to 7 percent of your body weight can help lower your risk of developing type 2 diabetes. So, if you’re 200 pounds, aiming to lose about 10 to 14 pounds might help you prevent prediabetes from progressing to full-blown type 2 diabetes or help halt the advancement of type 2 diabetes if you’ve already been diagnosed.
Drugs that increase insulin production by the pancreas or its blood levels and/or reduce sugar production from the liver, including alogliptin (Nesina), dulaglutide (Trulicity), linagliptin (Tradjenta), exenatide (Byetta, Bydureon), liraglutide (Victoza), lixisenatide (Adlyxin), saxagliptin (Onglyza), sitagliptin (Januvia), and semaglutide (Ozempic)
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.
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
Type 2 diabetes develops when the body cannot use insulin properly or make enough insulin, so the body cannot properly use or store glucose (a form of sugar) and sugar backs up into the bloodstream, raising blood sugar levels. In the United States, some 8.9 percent of adults 20 and older have been found to have diabetes, and health officials estimate that another 3.5 percent have undiagnosed diabetes.
Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
Like the sulfonylureas, meglitinides is a class of drugs that work by promoting insulin secretion from the pancreas. Unlike the sulfonylureas, which last longer in the body, repaglinide (Prandin) and nateglinide (Starlix) are very short acting, with peak effects within one hour. For this reason, they are given up to three times a day just before meals.
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