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How Does Metformin Work To Lower Blood Sugar

Posted at February 18th, 2023 | Categorised in Blood Sugar

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How Does Metformin Work To Lower Blood Sugar

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Metformin And Weight Loss: Can Metformin Be Used To Lose Weight?

By Malcolm J. Borg 1, 2, Christopher K. Rayner 1, Karen L. Jones 1, 2, Michael Horowitz 1, 2, Kong Xie 1 and Tongzhi Wu 1, 2, 3, *

Adelaide School of Medicine and Center for Research Excellence in Translating Nutrition Science into Better Health, University of Adelaide, Adelaide 5000, Australia

Received: November 6, 2020 / Revised: November 20, 2020 / Accepted: November 20, 2020 / Published: November 22, 2020

Metformin, the most widely prescribed drug for type 2 diabetes, has pleiotropic benefits in addition to lowering blood sugar levels, including reducing cardiovascular risk. The mechanisms underlying the latter remain unclear. Mechanistic studies to date have focused on the direct effects of metformin on the heart and blood vessels. Gastric effects are now recognized to be important for metformin’s glucose lowering. The gastrointestinal effects of metformin also have a major effect on cardiac function. This review summarizes the gastrointestinal mechanisms underlying the action of metformin and their potential relationship to cardiovascular benefits.

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Type 2 diabetes (T2D) is a key global health problem with increasing prevalence [1]. T2D is associated with a two- to three-fold increased risk of cardiovascular disease, the leading cause of death. Antidiabetic therapy focuses on lowering glucose, which, when effective, significantly reduces the risk of development and progression of microvascular complications (eg, neuropathy, retinopathy, nephropathy). However, improvements in glycemic control have only modest effects on macrovascular outcomes, with only a subset of antihyperglycemic agents associated with a beneficial effect on cardiovascular outcomes in T2D, including sodium-glucose-coupled transporter-2 (SGLT-2) inhibitors and glucagon . as peptide-1 (GLP-1) receptor agonists, with metformin [2].

Metformin is one of the oldest antidiabetic drugs and remains the first-line pharmacological treatment of T2D in many international guidelines [3]. Its pleiotropic effects, in addition to glucose lowering, include anti-obesity, anti-cancer, anti-aging and cardiovascular benefits. The latter, initially demonstrated in the UKPDS trial, is attracting increasing interest. In the UKPDS study, metformin use was associated with modest reductions in various cardiovascular endpoints and all-cause mortality, both with diet therapy alone and with intensive glucose-lowering therapy with replacement therapy in obese patients with T2D [4], 5]. These cardiovascular benefits have been confirmed in a number of subsequent studies [ 6 , 7 , 8 , 9 ], although neutral or harmful effects of metformin use in T2D have been reported in several studies [ 10 , 11 ]. .

Metformin is an effective fasting and postprandial glucose-lowering agent. The latter is significant as it represents an independent cardiovascular risk factor for subsequent hyperglycemia [12]. Changes in postprandial blood glucose, in particular, are strongly associated with the macrovascular complications of T2D [13], while rapid increases in postprandial blood glucose are associated with endothelial damage and initiation of a proatherogenic cascade [14, 15]. However, the cardiovascular benefits of metformin are generally considered to be mainly related to extraglycemic mechanisms. Mechanistic studies to date have focused on the direct effects of metformin on the heart and blood vessels. A variety of possible mechanisms have been identified, including changes in left ventricular function, reduction in ischemia-reperfusion injury, reduction in sympathetic activation and downregulation of adrenergic receptors, improvement in endothelial function, renin-angiotensin-aldosterone system, and changes in blood flow. Anti-stress and anti-inflammatory effect. Not surprisingly, the mechanisms that account for the cardiovascular benefits associated with metformin treatment remain controversial [16].

The antihyperglycemic mechanisms of metformin have historically been attributed to effects mediated after drug absorption, particularly hepatic glucose metabolism [17]. Recently, it has been increasingly recognized that the gastrointestinal tract is at least as important as the liver for metformin-induced glucose lowering [ 18 , 19 , 20 , 21 ]. In particular, a new delayed-release formulation of metformin, which releases its active ingredient in the lower jejunum and ileum, results in lower glucose levels than standard forms of metformin, despite minimal bioavailability [19, 22].

How Metformin Works For Pcos And Fertility

The possible effects of gastrointestinal effects of metformin on the cardiovascular system have been largely ignored [23]. This review summarizes the metabolic actions of metformin and their potential relevance to cardiovascular effects in T2D.

Metformin exhibits interrelated gastrointestinal effects of potential importance to cardiovascular function, including inhibition of bile acid resorption, modulation of gut microbiota, reduction of glucose absorption, enhancement of GLP-1 secretion and action, depletion of gases and retardation of gases. Reduction of blood pressure after a meal (Fig. 1) [23, 24].

Metformin reduces bile acid absorption in the ileum and therefore increases bile acid excretion in the faeces [25, 26]. Although bile acids are primarily recognized for their role in fat digestion, they interact with multiple receptors inside and outside the gastrointestinal tract [27]. In particular, bile acids activate Takeda G-coupled receptor 5 (TGR-5) and the farnesoid X receptor (FXR) perinuclear receptor. Increased TGR5 and decreased FXR activity are associated with inhibition of bile acid resorption [28]. Mechanistically, this could be explained by a decrease in bile acid absorption by enterocytes, leading to an increase in intestinal stimulation of membrane-bound receptors and a decrease in perinuclear receptor stimulation. Furthermore, altered bile acid synthesis—secondary to metformin-induced changes in the gut microbiota—increases the production of glucosodeoxycholic acid (GUDCA), a secondary bile acid that acts as an FXR antagonist [29]. Activation of the TGR5 receptor stimulates the release of GLP-1 from endocrine L-cells. This metformin potentiates bile acid-mediated GLP-1 secretion, cholecystokinin-induced GLP-1 secretion in healthy men receiving subcutaneous metformin treatment [30]. Bile acids may also contribute to metformin-enhanced GLP-1 secretion through their “escape” because enteroendocrine L-cells express different types of bitter taste receptors [31]. The potential cardiovascular effects of increased GLP-1 secretion are discussed later in this review. The FXR receptor is mainly present in organs exposed to high bile acid concentrations, for example the liver, kidney and gastrointestinal tract, but is also expressed in the arterial vasculature and heart [32]. Suppression of FXR-signaling can increase GLP-1 secretion [33] and has been reported to promote favorable cardiac remodeling in post-myocardial infarction [34].

Bile acids have several direct effects on systemic circulation, including negative chronotropy and inotropy, as well as antiapoptotic effects on cardiac myocytes, increasing nitric oxide production, modulating effects on angiogenesis, and reducing inflammation [35] . Although its effects on cardiovascular function remain unclear, studies of liver cirrhosis and bile acid sequestrants, a class of antidiabetic agents that bind to intestinal bile acids to prevent their reabsorption, point to the benefits of systemic reduction. Accumulation of bile acids. Systemic accumulation of bile acids in cirrhotic patients is associated with an array of adverse cardiac effects that constitute “cirrhotic cardiomyopathy.” In preclinical models, these changes have been shown to be reversible with the use of intestinal bile acid sequestrants [36, 37]. In addition, the decrease in plasma low-density lipoprotein cholesterol (LDL-C) reflects a decrease in the delivery of bile acids to the liver by bile acid sequestrants such as cholestyramine, thereby stimulating hepatic metabolism of cholesterol for bile acid synthesis [ 38]. Given the association of hypercholesterolemia with atherogenesis, bile acid extracts have been hypothesized to provide significant cardiovascular benefits, but adequately powered studies have shown that in most cases there is no cardiovascular benefit with these agents A trend toward reduced incidence [38 ]. Metformin lowers LDL-C levels, which should reduce the risk of heart disease; However, the LDL-C lowering effect of metformin is weaker than that of bile acid sequestrants (~6.5% with metformin vs 12% with cholestyramine).

Metformin: Uses, Side Effects And Cautions

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