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
If you have gestational diabetes, you should first try to control your blood glucose level by making healthy food choices and getting regular physical activity. If you can’t reach your blood glucose target, your health care team will talk with you about diabetes medicines, such as insulin or the diabetes pill metformin, that may be safe for you to take during pregnancy. Your health care team may start you on diabetes medicines right away if your blood glucose is very high.
Even if you aim to lose 5% of your body weight, if overweight, you are likely to see a fall in your blood glucose levels back into the normal range but even then we can’t say diabetes has been reversed or gone away. These actions build-up the body’s ability to respond to rising levels but if you get sick, eat more carbohydrate or gain some weight, more than likely your blood glucose levels will be on the rise again into the diabetes range.
Thank you Dr. Hallberg!! I am a Family Nurse Practitioner who did tele-medicine for 5 years before retiring. At 66 years of age my doctor diagnosed me with Type II Diabetes. I refused to take the medication and instead opted for a 6 month trial to lose enough weight to make the difference. After 4 months I’d lost 8 pounds and still had high blood sugars. Then my husband’s PCP recommended watching your TedTalk. That was the beginning and we both jumped into LCHF/Keto with both feet using Diet Doctor and you as our main resources. My husband has lost 38 pounds and I have lost 42 pounds since November 2017. More importantly my lab results today were a HgbA1c of 5.3 with average blood glucose of 105. I have about 50 more pounds to go to be at a healthier weight BUT I owe you a big thank you!! Now I’m working to encourage others of my friends, family and coaching clients to give LCHF/Keto a try! Thanks!!!!

Data from the Swedish randomized study of gastric banding showed that a loss of 20% body weight was associated with long-term remission in 73% of a bariatric surgery group, with weight change itself being the principal determinant of glucose control (13). Dietary weight loss of 15 kg allowed for reversal of diabetes in a small group of individuals recently receiving a diagnosis (21). In individuals strongly motivated to regain normal health, substantial weight loss is entirely possible by decreasing food consumption (88). This information should be made available to all people with type 2 diabetes, even though with present methods of changing eating habits, it is unlikely that weight loss can be achieved in those not strongly motivated to escape from diabetes. Some genetic predictors, especially the Ala12 allele at PPARG, of successful long-term weight loss have been identified (89), and use of such markers could guide future therapy. It must be noted that involuntary food shortage, such as a result of war, results in a sharp fall in type 2 diabetes prevalence (90,91).

Effect of an 8-week very-low-calorie diet in type 2 diabetes on arginine-induced maximal insulin secretion (A), first phase insulin response to a 2.8 mmol/L increase in plasma glucose (B), and pancreas triacylglycerol (TG) content (C). For comparison, data for a matched nondiabetic control group are shown as ○. Replotted with permission from Lim et al. (21).

This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
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).
You can talk to your diabetes health care team about making any necessary meal or medication adjustments when you exercise. They'll offer specific suggestions to help you get ready for exercise or join a sport and give you written instructions to help you respond to any diabetes problems that may happen during exercise, like hypoglycemia (low blood sugar), or hyperglycemia (high blood sugar).

Levels greater than 13–15 mmol/L (230–270 mg/dL) are considered high, and should be monitored closely to ensure that they reduce rather than continue to remain high. The patient is advised to seek urgent medical attention as soon as possible if blood sugar levels continue to rise after 2–3 tests. High blood sugar levels are known as hyperglycemia, which is not as easy to detect as hypoglycemia and usually happens over a period of days rather than hours or minutes. If left untreated, this can result in diabetic coma and death.

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.