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<blockquote data-quote="kokhongw" data-source="post: 1796167" data-attributes="member: 277199"><p>This 2009 paper by RA Defronzo has a section explaining what leads him to conclude in his abstract...</p><p><a href="http://diabetes.diabetesjournals.org/content/58/4/773" target="_blank">http://diabetes.diabetesjournals.org/content/58/4/773</a></p><p></p><p><strong>Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function.</strong></p><p></p><p>Here is a snippet:</p><p><span style="font-size: 15px"><strong>Sulfonylureas and metformin.</strong></span></p><p>Professor Robert Turner, in the UK Prospective Diabetes Study (UKPDS), was the first to conclusively show that sulfonylureas had no protective effect on the β-cell in newly diagnosed type 2 diabetic patients over the 15-year study duration (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-36" target="_blank">36</a>). After an initial drop in the A1C, sulfonylurea-treated patients experienced a progressive deterioration in glycemic control that paralleled the rise in A1C in the conventionally treated group (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#F15" target="_blank">Fig. 15</a>). Moreover, in the UKPDS sulfonylureas were shown not to have a significant protective effect against atherosclerotic cardiovascular complications (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-34" target="_blank">34</a>), and some studies even have suggested that sulfonylureas may accelerate the atherogenic process (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-276" target="_blank">276</a>,<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-277" target="_blank">277</a>). Similarly, metformin-treated patients in the UKPDS, after an initial decline in A1C, secondary to the biguanide's inhibitory effect on HGP, also experienced a progressive deterioration in glycemic control (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#F15" target="_blank">Fig. 15</a>) (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-278" target="_blank">278</a>). Using HOMA-β, Professors Holman and Turner showed that the relentless rise in A1C observed with both sulfonylureas and metformin resulted from a progressive decline in β-cell function and that by 3 years ∼50% of diabetic patients required an additional pharmacological agent to maintain the A1C <7.0% (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-279" target="_blank">279</a>–<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-284" target="_blank">284</a>). Although there is some in vitro evidence that metformin may improve β-cell function and prevent β-cell apoptosis (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-285" target="_blank">285</a>,<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-286" target="_blank">286</a>), the in vivo data from the UKPDS fail to support any role for metformin in the preservation of β-cell function. However, metformin was shown to reduce macrovascular events in UKPDS (<a href="http://diabetes.diabetesjournals.org/content/58/4/773#ref-278" target="_blank">278</a>), although by today's standards the number of diabetic subjects in the metformin arm (<em>n</em> = 342) would be considered inadequate to justify any conclusions about cardiovascular protection.</p></blockquote><p></p>
[QUOTE="kokhongw, post: 1796167, member: 277199"] This 2009 paper by RA Defronzo has a section explaining what leads him to conclude in his abstract... [URL]http://diabetes.diabetesjournals.org/content/58/4/773[/URL] [B]Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function.[/B] Here is a snippet: [SIZE=4][B]Sulfonylureas and metformin.[/B][/SIZE] Professor Robert Turner, in the UK Prospective Diabetes Study (UKPDS), was the first to conclusively show that sulfonylureas had no protective effect on the β-cell in newly diagnosed type 2 diabetic patients over the 15-year study duration ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-36']36[/URL]). After an initial drop in the A1C, sulfonylurea-treated patients experienced a progressive deterioration in glycemic control that paralleled the rise in A1C in the conventionally treated group ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#F15']Fig. 15[/URL]). Moreover, in the UKPDS sulfonylureas were shown not to have a significant protective effect against atherosclerotic cardiovascular complications ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-34']34[/URL]), and some studies even have suggested that sulfonylureas may accelerate the atherogenic process ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-276']276[/URL],[URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-277']277[/URL]). Similarly, metformin-treated patients in the UKPDS, after an initial decline in A1C, secondary to the biguanide's inhibitory effect on HGP, also experienced a progressive deterioration in glycemic control ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#F15']Fig. 15[/URL]) ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-278']278[/URL]). Using HOMA-β, Professors Holman and Turner showed that the relentless rise in A1C observed with both sulfonylureas and metformin resulted from a progressive decline in β-cell function and that by 3 years ∼50% of diabetic patients required an additional pharmacological agent to maintain the A1C <7.0% ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-279']279[/URL]–[URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-284']284[/URL]). Although there is some in vitro evidence that metformin may improve β-cell function and prevent β-cell apoptosis ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-285']285[/URL],[URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-286']286[/URL]), the in vivo data from the UKPDS fail to support any role for metformin in the preservation of β-cell function. However, metformin was shown to reduce macrovascular events in UKPDS ([URL='http://diabetes.diabetesjournals.org/content/58/4/773#ref-278']278[/URL]), although by today's standards the number of diabetic subjects in the metformin arm ([I]n[/I] = 342) would be considered inadequate to justify any conclusions about cardiovascular protection. [/QUOTE]
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