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.

Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.

Gene therapy can be used to manufacture insulin directly: an oral medication, consisting of viral vectors containing the insulin sequence, is digested and delivers its genes to the upper intestines. Those intestinal cells will then behave like any viral infected cell, and will reproduce the insulin protein. The virus can be controlled to infect only the cells which respond to the presence of glucose, such that insulin is produced only in the presence of high glucose levels. Due to the limited numbers of vectors delivered, very few intestinal cells would actually be impacted and would die off naturally in a few days. Therefore, by varying the amount of oral medication used, the amount of insulin created by gene therapy can be increased or decreased as needed. As the insulin-producing intestinal cells die off, they are boosted by additional oral medications.[76]
Reversal of type 2 diabetes to normal metabolic control by either bariatric surgery or hypocaloric diet allows for the time sequence of underlying pathophysiologic mechanisms to be observed. In reverse order, the same mechanisms are likely to determine the events leading to the onset of hyperglycemia and permit insight into the etiology of type 2 diabetes. Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking. Recent information on the intracellular effects of excess lipid intermediaries explains the likely biochemical basis, which simplifies both the basic understanding of the condition and the concepts used to determine appropriate management. Recent large, long-duration population studies on time course of plasma glucose and insulin secretion before the diagnosis of diabetes are consistent with this new understanding. Type 2 diabetes has long been regarded as inevitably progressive, requiring increasing numbers of oral hypoglycemic agents and eventually insulin, but it is now certain that the disease process can be halted with restoration of normal carbohydrate and fat metabolism. Type 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.
Known as gurmar, or “sugar destroyer,” in Aryuvedic medicine, Gymnema has consistently shown benefits in patients with diabetes. The most active part of Gymnema seems to be gymnemic acids, and many products list the percentage each capsule contains. Analyses of the herb for diabetes have shown it may be helpful in lowering high blood sugar levels. It can delay glucose absorption from the intestine. It was shown to regenerate pancreatic tissues, allowing more insulin to be produced, and help regulate insulin secretion. It also increases the utilization of glucose by the cell, reducing insulin resistance and decreasing appetite, especially for sweets. I usually use it in capsules, or in liquid form in some patients. Due to Gymnema having a very similar shape to glucose, it can fit into the taste bud receptors for sugar; it thus has unbelievable power to actually prevent the taste of sweets in the mouth for up to 1.5 hours. When I have a patient who is still struggling to not eat cake and cookies and so forth at parties or celebrations (or just in general), I will give her a tincture of Gymnema sylvestre. This is one of my favorite herbs for diabetes. In capsule form doses of 400 to 2,400 mg a day are recommended.
“The degree of carbohydrate restriction that we recommend to establish and then maintain nutritional ketosis depends upon individual factors such degree of insulin resistance (metabolic syndrome or type 2 diabetes?) and physical activity. These starting levels of carb restriction typically vary between 30 and 60 grams per day of total carbs. The best way to determine one’s carbohydrate tolerance is to directly measure blood ketones with a finger-stick glucometer that also accommodates ketone testing.

Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.


Blood sugar level is measured by means of a glucose meter, with the result either in mg/dL (milligrams per deciliter in the US) or mmol/L (millimoles per litre in Canada and Eastern Europe) of blood. The average normal person has an average fasting glucose level of 4.5 mmol/L (81 mg/dL), with a lows of down to 2.5 and up to 5.4 mmol/L (65 to 98 mg/dL).[7]
11. Get regular eye exams: Diabetic retinopathy is caused by elevated levels of blood sugar, which can happen when diabetes goes out of control. The disease can damage the blood vessels around the eye and retina, leading to blurred vision and blindness. Diabetic retinopathy cannot be cured, and often has no early symptoms, which makes it difficult to catch. Diabetics should make sure they get regular eye exams, for early detection and treatment.
Treatment for diabetes requires keeping close watch over your blood sugar levels (and keeping them at a goal set by your doctor) with a combination of medications, exercise, and diet. By paying close attention to what and when you eat, you can minimize or avoid the "seesaw effect" of rapidly changing blood sugar levels, which can require quick changes in medication dosages, especially insulin.
Pramlintide (Symlin) was the first in a class of injectable, anti-hyperglycemic medications for use in addition to insulin for type 1 diabetes or type 2 diabetes. Pramlintide is a synthetic analog of human amylin, a naturally occurring hormone made by the pancreas to help control glucose after meals. Similar to insulin, amylin is absent or deficient in person with diabetes.
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