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.
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.

For people with either type of diabetes, exercise can lower the chance of having a heart attack or stroke and can improve circulation. It may offer stress relief, as well. People with type 2 diabetes who need to lose weight can benefit from moderate exercise. Most people with diabetes are encouraged to get at least 150 minutes each week of moderate-intensity aerobic physical activity, like walking. Strength training is often recommended at least twice a week. Talk to your doctor about what type of exercise is right for you.


^ Jump up to: a b Safren, S.A., Gonzalez, J.S., Wexler, D.J., Psaros, C., Delahanty, L.M., Blashill, A.J., Margolina, A.I., & Cagliero, E. (2013). "A randomized controlled trial of cognitive behavioral therapy for adherence and depression (CBT-AD) in patients with uncontrolled type 2 diabetes". Diabetes Care. 37 (3): 625–33. doi:10.2337/dc13-0816. PMC 3931377. PMID 24170758.

I’m glad you talk about personal tolerance. My doc wants me to go on a ketogenic diet, but even when on the Autoimmune Paleo Diet, my adrenals would go a bit nuts. I can’t go any longer than 6 hours without food overnight…my adrenals start pumping out the adrenalin after about 3 to 6 hours of sleep (no matter what I eat or don’t eat before bed) and I wake up with anxiety. Adding a bit of carbs (3/4 cup at dinner and 1/2 cup at lunch) has allowed me to go a full 6 hours (would love 7 or 8) but it still feels terrible when I wake up.
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.

Gestational diabetes develops during pregnancy because hormones interfere with how the body uses insulin. When the pancreas can’t keep up with the insulin demand and blood glucose levels get too high, the result is gestational diabetes. About 2-7 percent of expectant mothers develop gestational diabetes during their pregnancy. Learn more about diabetes and pregnancy.


High blood sugar (hyperglycemia). Your blood sugar level can rise for many reasons, including eating too much, being sick or not taking enough glucose-lowering medication. Check your blood sugar level often, and watch for signs and symptoms of high blood sugar — frequent urination, increased thirst, dry mouth, blurred vision, fatigue and nausea. If you have hyperglycemia, you'll need to adjust your meal plan, medications or both.
Most lifestyle interventions focus on eating less and exercising more. But many patients have tried this and have seen minimal results, while also fighting unsustainable hunger and cravings. The problem with these programs is that they tend to be high in carbs, even if they are cutting back on calories. When you eat a high-carb diet, the resulting increase in your blood sugar triggers an insulin response in your body, and insulin blocks your body’s ability to burn fat. Insulin actively blocks the breakdown of stored body fat, meaning that as long as insulin is high, it will be very difficult to lose weight—even if you are eating very little.
Genetic factors do play a role in any disease, but I put this factor last for a reason. Genetic predisposition to a given disease will increase the chances of getting the disease, but not in a vacuum. People with a strong predisposition to liver disease manage to avoid it, and some with a family history of heart disease remain heart-attack free. Even studies among identical twins show that in most cases, twins will get the same diseases, even in different environments, but sometimes they don’t. This means there are other factors involved (see above).

Relying on their own perceptions of symptoms of hyperglycemia or hypoglycemia is usually unsatisfactory as mild to moderate hyperglycemia causes no obvious symptoms in nearly all patients. Other considerations include the fact that, while food takes several hours to be digested and absorbed, insulin administration can have glucose lowering effects for as little as 2 hours or 24 hours or more (depending on the nature of the insulin preparation used and individual patient reaction). In addition, the onset and duration of the effects of oral hypoglycemic agents vary from type to type and from patient to patient.
Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas. This release of insulin promotes the uptake of glucose into body cells. In patients with diabetes, the absence of insufficient production of or lack of response to insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.
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