This class of drugs pulls double-duty. The medicine in this class, colesevelam, lowers cholesterol and reduces blood sugar levels. So it could be a good choice if you have diabetes and high cholesterol levels. And because these drugs are not absorbed in the blood stream, they may be the best choice for someone who also has liver problems and cannot take some of the other diabetes medicines. Side effects from bile acid sequestrants can include constipation and flatulence (gas).
About the author:Mike Adams (aka the "Health Ranger") is a best selling author (#1 best selling science book on Amazon.com) and a globally recognized scientific researcher in clean foods. He serves as the founding editor of NaturalNews.com and the lab science director of an internationally accredited (ISO 17025) analytical laboratory known as CWC Labs. There, he was awarded a Certificate of Excellence for achieving extremely high accuracy in the analysis of toxic elements in unknown water samples using ICP-MS instrumentation. Adams is also highly proficient in running liquid chromatography, ion chromatography and mass spectrometry time-of-flight analytical instrumentation.
The prevalence of prediabetes is also on the rise, as it’s estimated that almost 34 million U.S. adults were prediabetic in 2015. People with prediabetes have blood glucose levels that are above normal but below the defined threshold of diabetes. Without proper intervention, people with prediabetes are very likely to become type 2 diabetics within a decade.
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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).
Type 2 diabetes results when the body is unable to produce the amount of insulin it needs to convert food into energy or when it is unable to use insulin appropriately. Sometimes the body is actually producing more insulin than is needed by a person to keep blood glucose in a normal range. Yet blood glucose remains high, because the body's cells are resistant to the effects of insulin. Physicians and scientists believe that type 2 diabetes is caused by many factors, including insufficient insulin and insulin resistance. They increasingly believe that the relative contribution each factor makes toward causing diabetes varies from person to person.
The earliest oral diabetes drugs were the sulfonylureas. These work by stimulating the pancreas to produce more insulin. The oldest of these drugs still on the market is chlorpropamide (Diabinese), which has been used for more than 50 years. The second-generation sulfonylureas are taken once or twice a day. They include glipizide (Glucotrol, Glucotrol XL), glyburide (Micronase, DiaBeta, Glynase), and glimepiride (Amaryl).
If you google “diabetes cure” you are directed to websites like WebMD and the Mayo Clinic where you find information on diet, exercise, medication, and insulin therapy, but nothing about the cure. This lack of information may have to do with the fact that Americans spend $322 billion a year to treat diabetes, $60 billion a year on weight-loss programs, and $124 billion a year on snack foods. This is about 3% of the US economy! Because so many peoples’ livelihoods are supported by diabetes and its main cause, obesity, the viral effect of people getting cured and telling others is greatly diminished.