Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCε and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCζ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.
This powerful herb promotes glucose utilization in the cells thus lowering blood glucose. It also prevents the liver from releasing more glucose into the blood stream, lowers cholesterol and triglycerides. Some people feel Gymnema Sylvestre is one of the most powerful herbs for treating high blood glucose – both type 1 and 2 diabetics. Also Gymnema Sylvestre may help rejuvenate beta cells in the pancreas thus helping heal the condition.
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.
Whole-body insulin resistance is the earliest predictor of type 2 diabetes onset, and this mainly reflects muscle insulin resistance (26). However, careful separation of the contributions of muscle and liver have shown that early improvement in control of fasting plasma glucose level is associated only with improvement in liver insulin sensitivity (20,21). It is clear that the resumption of normal or near-normal diurnal blood glucose control does not require improvement in muscle insulin sensitivity. Although this finding may at first appear surprising, it is supported by a wide range of earlier observations. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (27). Humans who have the PPP1R3A genetic variant of muscle glycogen synthase cannot store glycogen in muscle after meals but are not necessarily hyperglycemic (28). Many normoglycemic individuals maintain normal blood glucose levels with a degree of muscle insulin resistance identical to those with type 2 diabetes (29).
The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
Given the above research findings, it is recommended that drivers with type 1 diabetes with a history of driving mishaps should never drive when their BG is less than 70 mg/dl (3.9 mmol/l). Instead, these drivers are advised to treat hypoglycemia and delay driving until their BG is above 90 mg/dl (5 mmol/l). Such drivers should also learn as much as possible about what causes their hypoglycemia, and use this information to avoid future hypoglycemia while driving.
Lunch. Salads are always a good option for lunch – load it up with meat or tofu, cheese, avocado, veggies and a full-fat dressing like olive oil or ranch. In a rush? Grab a lettuce-wrapped burger or bread-less sandwich from any fast food outlet. Like to cook? Try steak and brussels sprouts smothered in butter, salmon and asparagus with hollandaise sauce or a Thai curry made with tofu, coconut milk and green beans.
“High glycemic index foods are going to be primarily processed foods,” says Lori Chong, RD, CDE, at The Ohio State University Wexner Medical Center in Columbus. Those processed foods tend to have more white sugar and flour in them, which are higher on the GI, she says. Foods lower on the GI include vegetables, especially non-starchy vegetables, like broccoli, cauliflower, and leafy greens and whole-grain products, such as brown rice (as opposed to white rice), Chong says. She notes that even many fruits are low on the GI, with pineapple and dried fruit being some of the highest (Berries, apples, and pears tend to be fairly low.)
The U.S. government’s study of the Diabetes Prevention Program found that in 3,000 people who had prediabetes, those who lost 5 percent to 7 percent of their body weight reduced their risk of developing Type 2 diabetes by 58 percent. The numbers were even more impressive in those over age 60. All study participants were overweight and had high blood sugar.
One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
Some people with type 2 diabetes can manage their disease by making healthy food choices and being more physically active. Many people with type 2 diabetes need diabetes medicines as well. These medicines may include diabetes pills or medicines you inject under your skin, such as insulin. In time, you may need more than one diabetes medicine to control your blood glucose. Even if you do not take insulin, you may need it at special times, such as during pregnancy or if you are in the hospital.
But is John “free of diabetes”? This is where the lines become blurred. Medically speaking, the term “cure” is usually associated with acute disease—a temporary medical condition, such as bacterial pneumonia, that can be cured with antibiotics. For diabetes, which is a chronic disease, it may be more accurate to use the term “remission” rather than cure. Particularly when considering the pathology associated with diabetes and the individual’s genetic predisposition, relapse is always possible. In a consensus statement issued by the ADA, the term remission is defined based on the following definitions:2
A patient diagnosed with type 2 diabetes (HbA1c of 6.5% or above) will always have type 2 diabetes. Interventions such as medication (including insulin), staying active and making good diet choices must be maintained to prevent the disease from progressing further. However, even if the patient undergoes strict medication, diet and exercise adherence and manages to lower the HbA1c they will still have type 2 diabetes.
Type 1 diabetes is commonly called “juvenile diabetes” because it tends to develop at a younger age, typically before a person turns 20 years old. Type 1 diabetes is an autoimmune disease where the immune system attacks the insulin-producing beta cells in the pancreas. The damage to the pancreatic cells leads to a reduced ability or complete inability to create insulin. Some of the common causes that trigger this autoimmune response may include a virus, genetically modified organisms, heavy metals, vaccines, or foods like wheat, cow’s milk and soy. (4)
Following these five principles can significantly influence blood glucose levels. However, not everyone responds the same. Some people with have immediate low blood glucose levels. Others may experience a slow and steady improvement of glucose control. Some may have temporary high glucose levels. Our experience is that this is transient and most people will improve.
Jump up ^ Tuomilehto, J; Lindström, J; Eriksson, JG; Valle, TT; Hämäläinen, H; Ilanne-Parikka, P; Keinänen-Kiukaanniemi, S; Laakso, M; et al. (2001). "Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance". The New England Journal of Medicine. 344 (18): 1343–50. doi:10.1056/NEJM200105033441801. PMID 11333990.
Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..