Controle de Sphaerotheca fuliginea em abobrinha com resíduo da fermentação glutâmica do melaço e produto lácteo fermentado.

O resíduo da fermentação glutâmica do melaço (RFGM), comercializado como fertilizante, foi inicialmente testado a 1,5% e a 2,5% em três formas: cru; esterilizado; e fermentado por Bacillus subtilis, a 30 e 50%, para o controle do Oídio (Sphaerotheca fuliginea) da abobrinha. Em outros dois experimentos os tratamentos foram: RFGM; suspensão contendo alguns aminoácidos existentes no RFGM; e suspensão de sais com concentrações próximas ao RFGM, pulverizados duas vezes por semana, a 2,5%. Também foi estudado o produto da fermentação do leite com Lactobacillus, pulverizado duas vezes por semana, nas concentrações de 10, 20, 30, 40 e 50%. Posteriormente, esse produto foi testado na concentração de 10%, aplicado uma e duas vezes por semana. Em todos os ensaios os tratamentos foram comparados ao fenarimol 0,1 ml/l e a água. No primeiro ensaio, o controle obtido foi de 99, 91, 98, 88, 94, 98 e 98%, respectivamente para fenarimol; RFGM a 1,5 e 2,5%; RFGM esterilizado a 1,5 e 2,5%; RFGM fermentado por B. subtilis 30 e 50%. Em outro experimento o RFGM, a suspensão de sais e de aminoácidos controlaram a doenca em 85%, 72% e 15%, respectivamente, apresentando a mesma tendência quando de sua repetição. As porcentagens de controle foram de 95, 99, 99, 99 e 99, com o produto lácteo, nas concentrações de 10, 20, 30, 40 e 50%, respectivamente. Quando esse mesmo produto foi aplicado uma e duas vezes por semana, o controle foi de 75% e 91%, respectivamente; e o controle com fungicida foi 84%

Long-term effects of bariatric surgery on meal disposal and beta-cell function in diabetic and nondiabetic patients.

Gastric bypass surgery leads to marked improvements in glucose tolerance and insulin sensitivity in obese type 2 diabetes; the impact on glucose fluxes in response to a physiological stimulus - such as a mixed meal (MTT) - has not been determined. We administered an MTT to 12 obese type 2 diabetic patients (T2D) and 15 obese nondiabetic subjects (ND) before and one year after surgery (10 T2D and 11 ND) using the double-tracer technique and modeling of ß-cell function. In both groups postsurgery, tracer-derived appearance of oral glucose was biphasic, a rapid increase followed by a sharp drop, a pattern that was mirrored by postprandial glucose levels and insulin secretion. In diabetic patients, surgery lowered fasting and postprandial glucose levels; peripheral insulin sensitivity increased in proportion to weight loss (∼30%), ß-cell glucose sensitivity doubled but did not normalize (viz. 21 nonsurgical obese and lean controls). Endogenous glucose production, however, was less suppressed during the MMT as the combined result of a relative hyperglucagonemia and the rapid fall in plasma glucose and insulin levels.We conclude that, in type 2 diabetes bypass surgery changes the postprandial response to a dumping-like pattern, improves glucose tolerance, ß-cell function, and peripheral insulin sensitivity but worsens endogenous glucose output in response to a physiological stimulus

Insulin Resistance in Humans Is Associated With Increased Plasma 12-Hydroxylated Bile Acids

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Human Insulin Resistance is Associated with Increased Plasma Levels of 12α-hydroxylated Bile Acids.

Bile acids (BAs) exert pleiotropic metabolic effects, and physicochemical properties of different BAs affect their function. In rodents, insulin regulates BA composition, in part by regulating the BA 12α-hydroxylase, Cyp8b1. However, it's unclear whether a similar effect occurs in humans. To address this question, we examined the relationship between clamp-measured insulin sensitivity and plasma BA composition in a cohort of 200 healthy subjects and 35 type 2 diabetes (T2D) patients. In healthy subjects, insulin resistance (IR) was associated with increased 12hydroxylated BAs (cholic acid, deoxycholic acid, and their conjugated forms). Furthermore, ratios of 12hydroxylated/non-12hydroxylated BA were associated with key features of IR including higher insulin, proinsulin, glucose, glucagon, and triglyceride levels, and lower HDL-cholesterol. In T2D patients, BAs were nearly twofold elevated, and more hydrophobic, compared to healthy subjects, though we did not observe disproportionate increases in 12hydroxylated BAs. In multivariate analysis of the whole dataset, controlling for gender, age, BMI, and glucose tolerance status, higher 12hydroxy/non-12hydroxy BA ratios were associated with lower insulin sensitivity and higher plasma triglycerides. These findings suggest a role for 12hydroxylated BAs in metabolic abnormalities in the natural history of T2D, and raise the possibility of developing insulin-sensitizing therapeutics based on manipulations of BA composition

Restored Insulin Inhibition On Insulin Secretion In Nondiabetic Severely Obese Patients After Weight Loss Induced By Bariatric Surgery.

To examine the impact of important weight loss on insulin inhibition of its own secretion during experimentally induced hyperinsulinemia under euglycemic conditions. Longitudinal, clinical intervention study--bariatric surgery (vertical banded gastroplasty--gastric bypass--Capella technique), re-evaluation after 4 and 14 months. Nine obese patients class III (BMI=54.6+/-2.6 kg/m2) and nine lean subjects (BMI=22.7+/-0.7 kg/m2). Euglycemic hyperinsulinemic clamp (insulin infusion: 40 mU/min m2), C-peptide plasma levels, electrical bioimpedance methodology, and oral glucose tolerance test (OGTT). BMI was reduced in the follow-up: 44.5+/-2.2 and 33.9+/-1.5 kg/m2 at 4 and 14 months. Insulin-induced glucose uptake was markedly reduced in obese patients (19.5+/-1.9 micromol/min kg FFM) and improved with weight loss, but in the third study, it was still lower than that observed in controls (35.9+/-4.0 vs 52.9+/-2.2 micromol/min kg FFM). Insulin-induced inhibition of its own secretion was blunted in obese patients (19.9+/-5.7%, relative to fasting values), and completely reversed to values similar to that of lean ones in the second and third studies (-60.8+/-4.2 and -54.0+/-6.1%, respectively). Weight loss in severe obesity improved insulin-induced glucose uptake, and completely normalized the insulin inhibition on its own secretion.27463-