Encellin’s ultra thin-film device won a $10,000 research prize in The American Diabetes Association's 22nd Annual Leaders Forum HealthTech Showcase in Northern California in late 2017. The company also won a 2016 Innovation Award from the San Francisco-based Rosenman Institute, an organization that aims to support the development of innovative medical-device technologies.
Many people have heard about type 2 diabetes, but its common precursor, prediabetes, doesn’t get as much attention. Prediabetes is estimated by CDC to affect 86 million Americans (51% of whom are 65 years and older), and an estimated 90% of people with prediabetes don’t even know it. According to the CDC, 15-30% of these individuals will develop type 2 diabetes within five years. In other words, as many as 26 million people that currently have prediabetes could develop type 2 diabetes by 2020, effectively doubling the number of people with type 2 diabetes in the US.
Answer: In recent years, intermittent fasting has emerged as a novel way of treating patients with type 2 diabetes. There are anecdotal reports of patients who have lost weight, their blood sugar levels have improved significantly, and they no longer need to take their diabetes medications. Their disease appears to be in remission – if not exactly cured.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
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One of my patients, aged 58, had an initial hemoglobin A1c of 7.2%. She was taking oral hypoglycemic agents, statins, and proton pump inhibitors—the basic treatment for every diabetes diagnosis. The patient was 28 lbs overweight and worked long hours. She didn’t exercise, mostly ate a processed food diet, and was sleep deprived. The patient had a family history of diabetes, and ultimately her lifestyle expressed her genetic tendencies.
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Use any combination of the tricks below to accelerate your weight loss and return to good health. If you use all five wisely, you can get to your ideal weight in 6–12 months or less — even if that means losing 100 pounds or more. Yes, think about your weight 10, 20, 30 years ago. Another friend of mine started on this journey last year weighing 270 pounds. He’s in his mid-thirties and about to reach his college wrestling weight class of 197 pounds and just ran his fastest 2 miles ever. He got to this point by following the two rules above and just 3 of the 5 tricks below.