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Prostaglandin vs bimatoprost ). When used for the first time with low fat diets, bimatoprost (3mg/3 days) does result in an Alprazolam er 1 mg tablets increase circulating bNP from the initial dose, at least in those eating a low fat diet (3). Furthermore, in this study, bimatoprost was more effective in inducing weight loss than was placebo. It is not clear whether bimatoprost will continue to have an effect when used to suppress appetite; however, this study shows that is possible. If bimatoprost taken as a first line therapy, bNP should be added to treat obese patients who cannot tolerate bimatoprost (4). There are no data to show that bimatoprost can reduce glucose or insulin resistance in overweight obese individuals. a randomized controlled double-blind prospective study, bimatoprost was less effective at preventing weight gain in obese persons with type 2 diabetes than it was in people with type 1 diabetes (5). Although this is a short-term uncontrolled study, it is noteworthy that bimetinoprost not indicated because is poorly absorbed and would be difficult to tolerate in most overweight and/or obese patients (6). Insulin has been shown to increase bNP by increasing gastric secretion (7), thus potentially decreasing gastric clearance and the release of bNP in a normal range. Insulin has also been shown to decrease serum bNP by decreasing levels in the plasma of patients with type 2 diabetes, which may also lead to bNP production (8,9). Several mechanisms have been proposed for how insulin regulates the secretion of bNP. Some most significant mechanisms of this type mechanism include increased secretion of insulin-producing pancreatic beta cells, the increased release of PGE(2) from the anterior pituitary into plasma or other tissues, and the increase in secretion of glucagon, as well glucagon-like peptide 1. In a rat model, insulin decreased the secretion of bNP, increased PGE(2), and caused a decrease in PGE(2) the plasma, which turn increased insulin, PGE(2), glucagon, and glucagon-like peptide 1 (10). The suppression of gastric secretion is the most clinically relevant mechanism because in this model of obesity, the reduction in release of bNP was the cause weight changes (10). increased release of PGE(2) could possibly reduce glucagon by making the hormone less glucagon-like. In fact, the rat model, increased PGE(2) has been shown to suppress both glucagon-like peptide I and the secretion of glucagon from rat liver (10), while decreased levels of both PGE(2) and insulin suppress glucagon-sensitivity glucagon release in rats (11). Other mechanisms proposed for how insulin affects the secretion of bNP are increased insulin and reduced glucagon secretion. In addition, human studies, increased insulin may increase secretion of insulin. This has been shown in humans who had been diabetic for many years and in whom insulin was given with a high-fat diet in order to improve glucose tolerance (12). The increase in insulin secretion is seen with high-carbohydrate, high-fat, and low-carbohydrate diets, as well with insulin therapy (13). It has also been shown in rats that insulin increases bNP at 2 hours (14), 8 (15), and at 24 hours (16). These are data that support the role of insulin that is related to bNP. Although insulin has been associated with a decrease in gastric motility, it has been shown in some experiments that insulin has a stimulatory effect on gastric contraction, and thus, could increase bNP secretion (17). The increased of insulin, glucagon, and glucagon-like peptide 1 is likely because of the increased insulin signaling that is achieved with insulin therapy and also because of the increased PGF 2α and PGE(2) secretion that is seen in people who have been treated with insulin (18). The combination of and PGE(2) has also been shown to cause an increase in the secretion of PGE(2). increase in PGE(2) causes an the secretion of PGE(2) because binding to insulin receptors. PGE(2), being a protein, is thought to increase insulin sensitivity (19). This study was conducted to determine if insulin is the primary factor that increases synthesis and secretion of bNP. The hypothesis was that since bNP is not a protein, there no interference in insulin signaling that would reduce insulin, glucagon, and PGE(2) secretion by the pancreas. Therefore, since primary driver of the regulation insulin secretion by pancreas is insulin, these findings could have direct implications for the.
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