Época de colheita e qualidade fisiológica de sementes de coentro produzidas no norte de Minas Gerais / Harvest season and physiological quality of coriander seeds produced in the north of Minas Gerais

No presente trabalho, objetivou-se avaliar a época de colheita e a qualidade fisiológica de sementes de coentro produzidas no Norte de Minas Gerais. A primeira época de colheita das sementes foi realizada aos 15 dias após o florescimento pleno, quando aproximadamente 50 por cento das plantas apresentavam flores. As demais colheitas foram realizadas de 7 em 7 dias, até as sementes atingirem 14,0 por cento de umidade, fato que ocorreu na 6ª colheita. Imediatamente após cada colheita, as sementes foram avaliadas quanto ao teor de água, à germinação e ao vigor (testes de primeira contagem, emergência de plântulas e índice de velocidade de emergência). A maturidade fisiológica das sementes de coentro, cultivar Verdão, ocorre entre 42 a 44 dias após o florescimento, quando as sementes apresentam umidade em torno de 28,0 por cento, podendo a colheita ser realizada até 50 dias após o florescimento, quando as sementes apresentavam 14,0 por cento de umidade.

The present study aimed to evaluate the harvest season and physiological quality of coriander seeds produced in the North of Minas Gerais. The first season of harvest of the seeds was performed 15 days after full bloom, when approximately 50 percent of plants had flowers. The other crops were carried out 7 in 7 days, until the seeds reach 14,0 percent moisture, a fact that occurred in the 6th harvest. Immediately after each harvest, the seeds were evaluated for water content, germination and vigor tests (first count, seedling emergence and emergence speed index). The physiological maturity of coriander seeds, cultivate Verdão, occurs between 42 to 44 days after flowering, when the seeds had humidity around 28,0 percent at physiological maturity, the harvest may be held until 50 days after flowering, when seeds had 14,0 percent humidity.

Effects of metformin on the glycemic control, lipid profile, and arterial blood pressure of type 2 diabetic patients with metabolic syndrome already on insulin

Fifty-seven type 2 diabetic patients with metabolic syndrome and on insulin were assessed by a paired analysis before and 6 months after addition of metformin as combination therapy to evaluate the impact of the association on glycemic control, blood pressure, and lipid profile. This was a historical cohort study in which the files of type 2 diabetic patients with metabolic syndrome on insulin were reviewed. The body mass index (BMI), waist circumference, lipid profile, A1C level, fasting blood glucose level, daily dose of NPH insulin, systolic blood pressure, and diastolic blood pressure were assessed in each patient before the start of metformin and 6 months after the initiation of combination therapy. Glycemic control significantly improved (P < 0.001) after the addition of metformin (1404.4 ± 565.5 mg/day), with 14 percent of the 57 patients reaching A1C levels up to 7 percent, and 53 percent reaching values up to 8 percent. There was a statistically significant reduction (P < 0.05) of total cholesterol (229.0 ± 29.5 to 214.2 ± 25.0 mg/dL), BMI (30.7 ± 5.4 to 29.0 ± 4.0 kg/m²), waist circumference (124.6 ± 11.7 to 117.3 ± 9.3 cm), and daily necessity of insulin. The reduction of total cholesterol occurred independently of the reductions of A1C (9.65 ± 1.03 to 8.18 ± 1.01 percent) and BMI and the reduction of BMI and WC did not interfere with the improvement of A1C. In conclusion, our study showed the efficacy of the administration of metformin and insulin simultaneously without negative effects. No changes were detected in HDL-cholesterol or blood pressure.

Non-obese adult onset diabetes with oral hypoglycemic agent failure: islet cell autoantibodies or reversible beta cell refractoriness?

Pancreatic ß cell function and insulin sensitivity, analyzed by the homeostasis model assessment, before and after 24 weeks of insulin therapy were studied and correlated with the presence of autoantibodies against ß cells (islet cell and anti-glutamic acid decarboxylase antibodies), in a group of 18 Brazilian lean adult non-insulin-dependent diabetes mellitus (NIDDM) patients with oral hypoglycemic agent failure (OHAF). Median fasting plasma glucose before and after insulin treatment was 19.1 and 8.5 mmol/l, respectively (P < 0.001); median HbA1c was 11.7 percent before vs 7.2 percent after insulin treatment (P < 0.001). Forty-four percent of the patients were positive (Ab+) to at least one autoantibody. Fasting C-peptide levels were lower in Ab+ than Ab- patients, both before (Ab+: 0.16 ± 0.09 vs Ab-: 0.41 ± 0.35 nmol/l, P < 0.003) and after insulin treatment (Ab+: 0.22 ± 0.13 vs Ab-: 0.44 ± 0.24 nmol/l, P < 0.03). Improvement of Hß was seen in Ab- (median before: 7.3 vs after insulin therapy: 33.4 percent, P = 0.003) but not in Ab+ patients (median before: 6.6 vs after insulin therapy: 20.9 percent). These results show that the OHAF observed in the 18 NIDDM patients studied was due mainly to two major causes: autoantibodies and ß cell desensitization. Autoantibodies against ß cells could account for 44 percent of OHAF, but Ab- patients may still present ß cell function recovery, mainly after a period of ß cell rest with insulin therapy. However, the effects of ß cell function recovery on the restoration of the response to oral hypoglycemic agents need to be determined

Cetoacidose diabética desencadeada por resistência imunológica à insulina / Diabetic ketoacidosis induced by immunologic insulin resistance

A cetoacidose diabética (CAD) é a emergência endocrinológica mais freqüente e de boa evoluçäo, na maior parte dos casos. Os autores apresentam evoluçäo atípica de três casos de CAD precipitada por resistência imunológica à insulina (RII). RELATO DE CASO. Três pacientes: H.M.L. (46 anos, diabetes mellitus (DM) tipo II, há 6 anos), D.R.J (39 anos, DM, secundário à pancreatopatia, há 11 anos) e D.L.S. (54 sanos, DM tipo II, há 9 anos) foram admitidos na Unidade de primeiro Atendimento do Hospital Säo Paulo em CAD: H.M.L. (glicemia: 716mg/dL, pH: 6,8), D.R.J. (glicemia: 684mg/dL, pH 6,.9) e D.L.S. (glicemia: 384mg/dL, pH: 7,2), todos apresentavam cetonúria. As necessidades de insulina para o controle metabólico foram: H.M.L.: 1.369UI, D.R.J.: 1.496UI, D.I.S. 1.369UI em, respectivamente: 212, 206 e 72 horas. Os anticorpos antiinsulina (AI) foram dosados por RE e ELISA: H.M.L.: 7.186nU/ml, 3,6IE; D.R.J.: 7,879nU/mL, 3,24IE; D.I.S: 8.377nU/mL, 2,88IE. O seguimento ambulatorial revelou queda progressiva dos níveis de AI:H.M.L.: 3.393nU/mL, 1,39, após dez meses da CAD; d.r.j.: 4,673Nu/Ml, 2,34 E d.i.s.: 1,510nU/mL, ambos após 18 meses da CAD. A queda nos níveis de anticorpos foi significativa nos três pacientes e foi acompanhada de melhor controle metabólico. Discussäo. A ausência de fator desencadeante, o elevado tempo, as altas doses de insulina empregadas para a compensaçäo metabólica levaram os autores à suspeita diagnóstica de RII. O diagnóstico foi confirmado pelos altos níveis séricos dos AI. O controle metabólico nestes pacientes foi obtido somente após a introduçäo de insulina na humanizada. CONCLUSAO. A resistência imunológica à insulina pode ser uma das causas de CAD sem fator precipitante aparente e má resposta às medidas terapêuticas habituais

Aspectos da fase näo-insulinodependente do diabetes mellitus do tipo I / Aspects of non-insulin-dependent phase of type I diabetes mellitus

Trata-se de um caso de diabetes mellitus do tipo I(DMI) no qual tivemos a oportunidade de diagnosticá-lo 23 meses antes das suas manifestaçöes clínicas mais freqüentes. Durante esse período foram observadas alteraçöes como o retorno de enurese, diminuiçäo na velocidade de crescimento e episódios de hiperglicemia e/ou glicosúria transitórios, apresentadas pela paciente, que podem näo ser devidamente valorizadas, na rotina clínica. Como, também, o aparecimento de marcadores imunológicos (ICA) e alteraçöes precoces na secreçäo de insulina (diminuiçäo na sua primeira fase de liberaçäo) vários meses antes do DMI manifesto. Esses marcadores imunológicos e essas alteraçöes endócrinas deveriam, se possível, ser pesquisados em pacientes com o quadro clínico inicial aqui apresentado, e em parentes jovens de DMI, no sentido de se detectar indivíduos com elevado risco de evoluírem para a fase manifesta dessa moléstia. O seguimento desses pacientes possibilitaria o diagnóstico precoce do DMI e a aplicaçäo de medidas no sentido de impedir a deteriorizaçäo total das células beta-pancreáticas e a evoluçäo para distúrbios metabólicos mais graves, como a cetoacidose diabética, com morbidade e mortalidade reconhecida

Insulin autoantibodies in first degree relatives of type I diabetic patients

Insulin autoantibodies (IAA) of first-degree relatives of type diabetic patient and recent-onset type I diabetics were measured by radioimmunoassay. A cut-off of 60 nU/ml was established on the basis of the values of normal control individuals. The intra-assay coefficient of variation was 9.2% for a moderately positive serum (1908 ñ 176 nU/ml (mean ñ SD), N=7; range, 1708 to 2158 nU/ml). The interassay coefficient of variation was 23.8% for a negative (normal control) serum (28.1 ñ 6.7 nU/ml, N=6; range, 22 to 39 nU/ml) and 14.5% in a highly positive serum (6185 ñ 899 nU/ml, N=7; range, 5053 to 7009 nU/ml). Insulin autoantibody levels (mean ñ SEM) were 19.3 ñ 2.8 nU/ml (range, =-19 to 40 nU/ml) in 25 controls, 24.8 ñ 3.4 nU/ml (range, -17 to 59 nU/ml) in 41 type II diabetic patients, 18.5 ñ 2.4 nU/ml (range, -58 to 268 nU/ml) in 171 first-degree relatives of type I diabetic patients and 208.9 ñ 87.0 nU/ml (range, 10 to 1101 nU/ml) in 16 recent-onset type I diabetic patients. IAA levels were significantly higher in the last group compared with the other groups (P<0.01). None of the controls or type II diabetics exceeded the upper limit of normalyity. In contrast, 9 of 171 (5.3%) first-degree relatives and 9 of 16 (56.0%) recent-onset type I diabetic patients had IAA levels above the 60 nU/ml cut-off point. These data indicate that this method is effective for the detection of individuals who are at high risk to develop type I diabetes

Relationship between insulin antibodies and metabolic control in type I diabetes mellitus

1. The objective of the presente study was to investigate whether a change in insulin therapy from bovine to purified porcine insulin would result in a decreased level of insulin antibodies (IA) in type I diabetic patients and whether there would be better metabolic control. 2. Insulin antibodies were measured by ELISA. Fifteen type I diabetic patients were prospectively followed for 8 months with monthly evaluations after changing insulin therapy from bovine to purified porcine insulin. 3. Group I patient (N = 4) had > ou = 1.5 (value obtained by dividing the ELISA absorbande of the tested serum by the absorbance of a standard serum) at the beginning of the study. For group I patients, the modification of insulin therapy caused a 57% reduction in insulin antibody levels, and this reduction was correlated with a decrease in 24-hour glycosuria (rs = 0.66, P < 0.001) and glicated protein (rs = 0.65, P < 0.01). Group II patients (N = 8) had IA < 1.5 and > ou = 0.3 and group III (N = 3 had IA < 0.3. Insulin antiblody levels were unchanged during the follow-up period in both group II and group III. 4. We also studied endogenous insulin secretion, measured as fasting C-peptide, and its relationships with metabolic control and insulin antibody levels. Patient with residual insulin secretion (C-peptide > 60 pmol/l) showed lower levels of 24-h glycosuria, glycated protein and glycated hemoglobin. Furthermore, in this group of patients a negative correlation was found between C-peptide and insulin antibody levels (rs=0.36, P < 0.01). 5. We conclude that insulin antibodies could be one of the factors having a detrimental effect on metabolic control