I bring this up because sleep apnea increases a person’s risk for developing type 2 diabetes. Also, sleep-disordered breathing is also related to proper nutrition throughout life. And perhaps most importantly, the first line of defense in catching sleep-disordered breathing in patients early, are dentists. This is another area where dentists must get involved if we want to tackle the issue of pervasive type 2 diabetes with any success.
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.
If this means I can get an A1c of 6.5 without any insulin then that would be great in my case. I’m type 1 diabetic that has to exercise after my meals to get my blood sugar levels down. Having a low due to insulin causes severe problems due to chronic sinus infections that won’t go away due to diabetes. I bike 31 miles after my 1st meal and walk 5 mile after my next meal which allows me to keep my insulin usage very low for a type 1. It would be a big help in my case even… Read more »
Professor Andrew Hattersley, a Consultant in Diabetes at the Royal Devon and Exeter Hospital and Research Professor at the University of Exeter Medical School, looked forward. "Now we know there is a "seven year switch," the next question is why? Has the immune attack stopped or are we left with "super beta-cells" that can resist the immune onslaught. Any insights into halting the relentless destruction of the precious insulin-producing cells are valuable. We could not have made this progress without the help of over 1,500 patients. We owe it to them to try to find answers that might help patient care quickly."
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.
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Efforts to cure or stop type 1 diabetes are still in the early stages, and these approaches will also not be suitable for people that have already lost their insulin-producing cells. A solution could be the creation of an “artificial pancreas” — a fully automated system that can measure glucose levels and inject the right amount of insulin into the bloodstream, just like a healthy pancreas would.