Is a prediabetes diagnosis serious? There has been significant debate around the term ‘prediabetes,’ and whether it should be considered cause for alarm. On the one hand, it serves as a risk factor for type 2 diabetes and a host of other complications, including heart disease, and ultimately prediabetes implies that a degree of metabolic problems have started to occur in the body. On the other hand, it places a diagnosis on many people who may never develop type 2 diabetes. Again, according to the CDC, 15-30% of those with prediabetes will develop type 2 diabetes within five years. However, a 2012 Lancet article cites 5-10% of those with prediabetes each year will also revert back to healthy blood sugars.
Rosiglitazone (Avandia) and pioglitazone (ACTOS) are in a group of drugs called thiazolidinediones. These drugs help insulin work better in the muscle and fat and also reduce glucose production in the liver. The first drug in this group, troglitazone (Rezulin), was removed from the market because it caused serious liver problems in a small number of people. So far rosiglitazone and pioglitazone have not shown the same problems, but users are still monitored closely for liver problems as a precaution. Both drugs appear to increase the risk for heart failure in some individuals, and there is debate about whether rosiglitazone may contribute to an increased risk for heart attacks. Both drugs are effective at reducing A1C and generally have few side effects.
Known for its immune-boosting and disease-fighting benefits, this Chinese herb has several positive diabetes studies behind it. Researchers have found that ginseng slows carbohydrate absorption; increases cells’ ability to use glucose; and increases insulin secretion from the pancreas. A team from the University of Toronto has repeatedly demonstrated that ginseng capsules lower blood glucose 15 to 20 percent compared to placebo pills. These are the best superfoods for people with diabetes.
An insulin pump is a small machine that gives you small, steady doses of insulin throughout the day. You wear one type of pump outside your body on a belt or in a pocket or pouch. The insulin pump connects to a small plastic tube and a very small needle. You insert the needle under your skin and it stays in place for several days. Insulin then pumps from the machine through the tube into your body 24 hours a day. You also can give yourself doses of insulin through the pump at mealtimes. Another type of pump has no tubes and attaches directly to your skin, such as a self-adhesive pod.
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.
Glucose in the bloodstream passes through the kidneys, where it can either be excreted or reabsorbed. Sodium-glucose transporter 2 (SGLT2) works in the kidney to reabsorb glucose, and a new class of medication, SGLT2 inhibitors, block this action, causing excess glucose to be eliminated in the urine. Canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance) are SGLT2 inhibitors that have been approved by the FDA to treat type 2 diabetes. Because they increase glucose levels in the urine, side effects can include urinary tract and yeast infections.
Dr Beverley Shields, at the University of Exeter Medical School, who led the research, said: "This finding is really exciting. It suggests that a person with Type 1 diabetes will keep any working beta-cells they still have seven years after diagnosis. We are not sure why this is; it may well be that there is a small group of "resilient" beta-cells resistant to immune attack and these are left after all the "susceptible" beta-cells are destroyed. Understanding what is special about these "resilient" beta-cells may open new pathways to treatment for Type 1 diabetes."
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In type 1 diabetes, patients sometimes experience what physicians have come to call a "honeymoon period" shortly after the disease is diagnosed. During the "honeymoon period" diabetes may appear to go away for a period of a few months to a year. The patient's insulin needs are minimal and some patients may actually find they can maintain normal or near normal blood glucose taking little or no insulin.
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.
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).
Trick (important): Cut down on sweets, and if you can, cut them out entirely for a couple months. I still eat ice cream about once a week, and know people who are losing weight on this diet while eating ice cream almost every day. But this probably won’t be the case for everyone. Better to severely restrict sweets for the first few months, and then gradually reintroduce.