I’ve re-posted the lastest medical article from medscape on Bariatric Surgery in Diabetes Mellitus.  As many of you know, I have a special interest in Bariatrics/ Diabetes due to the increased incidence of cardiovascular complications.  However, here in the USA – it’s easier to get cardiac bypass surgery then gastric bypass..

So – instead of helping people with real medical problems – we wait for drastic complications (heart attacks etc.)  Even then, society in general and medical society in particular can be rather judgemental about obese patients.  In stead of judging – make the information more available, and give people an opportunity to decide for themselves.

This is a straight cut and paste, with no editing or editorializing (except my comments above) for my interested readers.  Also – please let me know what other surgical procedures you are interested in hearing about and I will post articles with helpful information.

Authors and Disclosures :Journalist Daniel M Keller, PhD Daniel M. Keller is a freelance writer for Medscape. Daniel M. Keller has no disclosures.

From Medscape Medical News:

 Remission of Type 2 Diabetes Can Occur Within a Week of Gastric Bypass Surgery

Daniel M. Keller October 1, 2010 (Stockholm, Sweden) — Twelve patients with type 2 diabetes had improvements in insulin sensitivity and beta cell function just 1 week after Roux-en-Y gastric bypass surgery (RYGB), with concomitant reductions in fasting and 2-hour postprandial plasma glucose levels, compared with preoperative levels, according to a poster presentation here at the European Association for the Study of Diabetes 46th Annual Meeting. Lead author Nils Bruun Jørgensen, MD, from the Department of Endocrinology at Hvidovre Hospital in Denmark, showed evidence that the improvements in insulin sensitivity and beta cell function were associated with a 16-fold increase in secretion of glucagon-like peptide 1 (GLP-1). Type 2 diabetes patients with fasting plasma glucose of more than 7.0 mmol/L at the beginning of the study were given a mixed-meal tolerance test 1 to 3 days before and 4 to 6 days after surgery. The 200 mL, 1260 kJ liquid meal provided 15% of energy from protein, 50% from carbohydrate, and 35% from fat. The average age of the patients was 51.8 years, 7 were male, and they had diabetes for an average of 5.2 years. Significant reductions in fasting and in 120-minute postprandial plasma glucose levels occurred after surgery, compared with preoperative values (see table). Similarly, there were decreases in both fasting insulin and C-peptide serum levels. Subject Characteristics and Laboratory Values Before and After RYGB Surgery Variables Pre-RYGB Post-RYGB Change P value Glycated hemoglobin 7.0 ± 0.3 Fasting plasma glucose (mmol/L) 8.8 ± 0.7 7.0 ± 0.3 –21.2% .005 120-min plasma glucose (mmol/L) 11.4 ± 0.8 8.2 ± 0.7 –28.5% <.001 Fasting serum insulin (pmol/L) 132 ± 22 73 ± 9 –44.6% .006 Fasting serum C-peptide (pmol/L) 1542 ± 151 1175 ± 172 –23.8% <.001 Weight (kg) 129.8 ± 4 127 ± 3.8 –2.2% .001 Body mass index (kg/m2) 43.3 ± 1.5 42.4 ± 1.5 –2.1% .001 Waist (cm) 130.8 ± 2.9 131.3 ± 2.6 0.4% .734 Hip (cm) 121.0 ± 2.9 118 ± 2.7 –2.5% .051 Using the homeostasis model assessment of insulin resistance (HOMA-IR), Dr. Jørgensen determined that insulin resistance decreased by 54%, from 6.9 ± 1.0 before to 3.2 ± 0.43 after RYGB (P = .001). The Matsuda Index, a measure of tissue insulin sensitivity, increased in parallel with the decrease in insulin resistance, going from 2.58 ± 0.38 before to 4.16 ± 0.55 after RYGB (P = .01). “We also looked at the C-peptide levels in response to the meal, and although we couldn’t show any significant difference in the individual postprandial sample points, what we did get was an impression of the changed secretion dynamics, and we could show an increased incremental area under the curve for C-peptide,” he said. The area under the curve of concentration for C-peptide over time increased significantly after surgery (P = .04). The disposition index, a measure of the relation between the sensitivity of beta cells to glucose and tissue sensitivity to insulin, “improved dramatically,” according to the investigators. “We found a significant increase in the beta cell function, and when we related this to the ambient insulin resistance, we found a 3-fold increase in the disposition index,” according to Dr. Jørgensen — from 54 ± 12 before to 157 ± 30 after RYGB (P = .001). To determine the underlying cause of these improvements, the researchers investigated secretion of incretins, and “found a significant and very dramatic increase in the GLP-1 secretion after surgery,” he said. GLP-1 peak plasma levels increased 5.6-fold after surgery, compared with preoperative values (P < .001), and the incremental area under the curve for plasma GLP-1 was 16 times greater after than before RYGB (P < .001). There was no observed change in gastric inhibitory polypeptide. In conclusion, “gastric bypass surgery significantly reduced fasting plasma glucose levels and 2-hour postprandial glucose levels. These changes were associated with increased insulin sensitivity and beta cell function, and may involve the increased secretion of GLP-1,” Dr. Jørgensen told the audience. Discussion leader Ele Ferrannini, MD, professor of medicine at the University of Pisa Medical School in Italy, asked Dr. Jørgensen about the potential influence of caloric deprivation on the findings, “which would mimic these data almost perfectly,” Dr. Ferrannini said. Dr. Jørgensen replied that he could not dissect such a proposed mechanism from the results he saw after RYGB. Dr. Ferrannini noted that the literature contains studies of patients with type 2 diabetes who were subjected to low-calorie diets in the range used in this study. “And their findings, with the exception of the release of GLP-1, were precisely what is here, so this is a confounder in this particular finding,” he said. An audience member noted that the patients in this study had diabetes for an average of a little more than 5 years, and wondered what would be the result if one performed RYGB on patients who had their disease and had been on insulin much longer, in essence, questioning whether there would be enough preserved beta cell function to see effects similar to those in this study. Dr. Ferrannini replied that “there is evidence that . . . the longer the duration of diabetes, . . . the lower the remission rate, particularly if you look a year later. Any diabetic will go into remission if you starve them, but when they start eating again [after they lost weight], a year later or 2 years later, some will be in remission, others will not be in remission or will be halfway between remission and nonremission. Those that have had the disease the longest . . . may relapse if they remitted initially.” “And then to the point of the insulin secretion — it’s true that it’s not really very much higher, but this is in the face of lower glucose levels. So if you construct a kind of relationship between the insulin and the concomitant glucose levels, there will be an input, and this can be attributed also to the GLP-1. What you cannot ascribe to the increased GLP-1 levels is any improvement in insulin sensitivity, because of a lack of evidence that GLP-1 has any influence on insulin action,” Dr. Ferrannini said.

Dr. Jørgensen reports that his doctoral studies were partially funded by Novo Nordisk, and that 2 of his coauthors are Novo Nordisk employees. Dr. Ferrannini has disclosed no relevant financial relationships. European Association for the Study of Diabetes (EASD) 46th Annual Meeting: Abstract 668. Presented September 23, 2010. Medscape Medical News © 2010 WebMD, LLC