There are two medicines in this group: repaglinide and nateglinide. Both of these lower your blood glucose by prompting the pancreas to release more insulin. These drugs work quickly and do not stay in your system long. So they are a good option if your meal schedule varies or is unpredictable. They also cause less weight gain that other oral diabetes medicines.
Khodneva, Y., Shalev, A., Frank, S. J., Carson, A. P., & Safford, M. M. (2016, May). Calcium channel blocker use is associated with lower fasting serum glucose among adults with diabetes from the REGARDS study. Diabetes Research and Clinical Practice, 115, 115-121. Retrieved from http://www.diabetesresearchclinicalpractice.com/article/S0168-8227(16)00070-X/abstract
Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).

Type 1 diabetes is a particularly unpleasant condition. It occurs when the pancreas ceases to produce the insulin needed by the body to metabolize sugar and, until the invention of artificial insulin injections, it was as deadly as cancer. Type 2 is the less severe form of the disease, where the body produces insufficient insulin; it can often be managed through diet alone.
A substantial proportion of people who experience type 2 diabetes remission after gastric bypass eventually have relapse of the disease down the road. I feel the best study of this was done by my co-author on CROSSROADS, David Arterburn. In a study of nearly 5,000 patients with diabetes who underwent [gastric bypass surgery] and were followed retrospectively for 13 years, about 70% experienced diabetes remission. Among these, about 1/3 eventually relapsed, but it’s important to note that the median disease-free interval was 8.3 years.
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.

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.

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