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Background: Obesity surgery is an effective method for treating obesity and diabetes mellitus type 2. This type of diabetes can be completely resolved in 78.1% of diabetic patients and can be improved or resolved in 86.6% of diabetic patients. But little is known about bariatric surgery in type 1 diabetes mellitus. Methods: We report of 6 female obese patients with diabetes mellitus type 1 who had bariatric surgery. Two of them underwent Roux-en Y gastric bypass (RNYGB), one of them had sleeve gastrectomy and the remaining three had biliopancreatic diversion with duodenal-switch (BPD-DS). Results: Our results showed a remarkable weight reduction as well as an improvement in their blood glucose control and the insulin requirement in the follow-up years after surgery. Pre-surgery the BMI of our 6 patients ranged between 37.3-46.0 kg/m² and improved to 25.8-29.0 kg/m² one year after surgery. HbA1c decreased from 6.7-9.8% presurgery to 5.7-8.5% after one year postsurgery. The total amount of daily insulin requirement was reduced from 62-150 IU/day presurgery to 1554 IU/day after one year. Conclusion: The results are impressive and show an improvement in insulin sensitivity following obesity surgery. However, an optimal blood glucose control still remains very important in the therapy of diabetes mellitus type 1 to avoid long-term-complications. Introducción: La cirugía de la obesidad es un método eficaz para el tratamiento de la obesidad y la diabetes mellitus tipo 2. Este tipo de diabetes puede se resuelve por completo en el 78,1% de los pacientes diabéticos y mejora en el 86,6% de los pacientes diabéticos. Sin embargo, poco se sabe acerca de la cirugía bariátrica en la diabetes mellitus tipo 1. Métodos: Presentamos 6 pacientes mujeres obesas con diabetes mellitus tipo 1 que se sometieron a cirugía bariátrica. Dos de ellas fueron sometidas a un bypass gástrico en-Y-Roux (BPGYR), una se le realizó una gastrectomía en manga y a las tres restantes una derivación biliopancreática con switch duodenal (DBP-SD). Resultados: Nuestros resultados mostraron una reducción de peso notable, así como una mejora en el control de la glucosa en sangre y el requerimiento de insulina en los años de seguimiento después de la cirugía. El IMC prequirúrgico de las 6 pacientes osciló entre 37,3-46,0 kg/m² y mejoró a 25,8-29,0 kg/m² un año después de la cirugía. La HbAlc disminuyó de 6,7-9,8% antes de la cirugía a 5,7-8,5% un año después de la cirugía. El requerimiento diario de insulina se redujo de 62-150 UI/día antes de la cirugía a 15-54 UI /día al cabo de un año. Conclusión: Los resultados son impresionantes y muestran una mejora en la sensibilidad a la insulina tras una cirugía de la obesidad. No obstante, un control óptimo de la glucosa de sangre sigue siendo muy importante en la terapia de la diabetes mellitus tipo 1 para evitar complicaciones a largo plazo.

In 1928, Frey and co-workers discovered kallikrein in human urine and described its prolonged hypotensive effect in the dog. Four years later, the same authors first reported a blood glucose-lowering effect of orally administered kallikrein in diabetic patients. However, the observed blood glucose-lowering effect of kallikrein appeared to fade with repeated administration, and therefore its possible metabolic role was not further investigated and fell into disregard. One decade ago, experimental data yielded indirect evidence that the regulation of local skeletal muscle blood flow and glucose uptake during work was mediated by proteolytically cleaved kinins. Further experiments demonstrated that in insulin-resistant states such as postoperative stress and type II diabetes, reduced muscular insulin sensitivity was increased and partly restored by continuous low-dose infusion of synthetic bradykinin. Recent work showing that tissue kallikrein is present in a number of different tissue sites, including skeletal muscle and our own observation of local kinin overflow after muscle work in healthy subjects, but not in type II diabetics, support the concept of a skeletal muscle kallikrein-kinin system (KKS) that is locally activated upon contraction. Moreover, in isolated perfused rat heart preparations, favorable effects of kinins on myocardial glucose uptake, oxidation, and glycolytic flux have been reported. Most interestingly, cardioprotective effects of kinins have been observed and attributed to improved energy and substrate metabolism in ischemic hearts. Taken together, these data gave rise to the concept that tissue KKS might be involved in the local modulation of skeletal muscle and myocardial tissue blood flow and substrate metabolism, and that activation of the KKS is defective in insulin-resistant states.

Angiotensin-converting enzyme (ACE) inhibitor-stimulated glucose metabolism and perfusion in muscle tissue seem to be, at least in part, mediated by kinins. However, the relative contribution of direct metabolic or secondary hemodynamically induced effects is unclear, It was the aim of this study to characterize the effects of ACE inhibition and bradykinin on glucose transport while changes in cardiocoronary function that might influence glucose transport were minimized. Hearts from Wistar rats were perfused by a Langendorff preparation and a set of functional parameters were simultaneously measured, Bradykinin (10(-11) M) and fosinoprilate (10(-7) M) were administered at concentrations that did not affect coronary flow, Insulin was employed as reference at half-maximal concentration, The nonmetabolizable glucose analog 3-O-[C-14]methyl-D-glucose and the nontransportable tracer L-[H-3]glucose were coperfused for the calculation of glucose transport. Using a 2-compartment mathematical model we found that the glucose transport rate, which was doubled with insulin, was increased almost 3-fold by either bradykinin or fosinoprilate. In the presence of the B-2 bradykinin receptor antagonist HOE 140 (D-Arg[Hyp(3),Thi(5), D-Tic(7),Oic(8)]-bradykinin; icatibant), the effect of both agents was completely abolished, Both agents also induced minor changes in contractility/relaxation parameters that again were completely neutralized with icatibant, A perfusion-independent but B-2-kinin receptor-dependent stimulating effect on glucose transport by either bradykinin or fosinoprilate is concluded, This effect could, in analogy to insulin be due to increased glucose transporter translocation, increased endothelium-derived nitric oxide formation, or-despite constant coronary flow conditions-secondary to altered cardiac function. (C) 1997 by Excerpta Medico, Inc.

The converting enzyme not only converts angiotensin I into angiotensin II but also metabolizes bradykinin. Furthermore, the effects of ischemia on myocardial tissue damage can be modulated by converting enzyme inhibitors. It is unknown whether these effects of ACE-inhibitors are due to increased bradykinin production. In this paper we describe the effects of captopril on bradykinin production in the ischemic isolated rat heart. The reduced deleterious effects of ischemia by captopril were associated with a stimulated bradykinin production. Beneficial effects of bradykinin could be due to an improved perfusion or to an effect on cellular metabolism. Therefore, we conclude that this effect on kinins by ACE-inhibitors is of importance in modulating tissue damage during ischemia.