Restored insulin inhibition on insulin secretion in nondiabetic severely obese patients after weight loss induced by bariatric surgery.

OBJECTIVE: To examine the impact of important weight loss on insulin inhibition of its own secretion during experimentally induced hyperinsulinemia under euglycemic conditions. DESIGN: Longitudinal, clinical intervention study--bariatric surgery (vertical banded gastroplasty--gastric bypass--Capella technique), re-evaluation after 4 and 14 months. SUBJECTS: Nine obese patients class III (BMI=54.6+/-2.6 kg/m2) and nine lean subjects (BMI=22.7+/-0.7 kg/m2). MEASUREMENTS: Euglycemic hyperinsulinemic clamp (insulin infusion: 40 mU/min m2), C-peptide plasma levels, electrical bioimpedance methodology, and oral glucose tolerance test (OGTT). RESULTS: 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). CONCLUSION: Weight loss in severe obesity improved insulin-induced glucose uptake, and completely normalized the insulin inhibition on its own secretion.

Lack of insulin inhibition on insulin secretion in non-diabetic morbidly obese patients.

OBJECTIVE: Insulin inhibition of insulin secretion has been described in normal lean subjects. In this study, we examined whether this phenomenon also occurs in the morbidly obese who often have severe peripheral insulin resistance. SUBJECTS: Twelve obese patients, normotolerant to glucose (8 F/4 M, body mass index (BMI)=54.8+/-2.5 kg/m(2), 39 y) and 16 lean control subjects (10 F/6 M, BMI=22.0+/-0.5 kg/m(2), 31 y). DESIGN AND MEASUREMENTS: An experimental study using various parameters, including an euglycemic hyperinsulinemic clamp (280 pmol/min/m(2) of body surface), an oral glucose tolerance test (OGTT), electrical bioimpedance and indirect calorimetry. RESULTS: The obese subjects were insulin resistant (M=19.8+/-1.6 vs 48.7+/-2.6 micromol/min kg FFM, P<0.0001) and hyperinsulinemic in the fasted state and after glucose ingestion. Fasting plasma C-peptide levels (obese 1425+/-131 pmol/l vs lean 550+/-63 pmol/l; P<0.0001) decreased less during the clamp in the obese groups (-16.9+/-6.9% vs -43.0+/-5.6% relative to fasting values; P=0.007). In the lean group, the C-peptide decrease during the clamp (percentage variation) was related to insulin sensitivity, M/FFM (r=0.56, P=0.03), even after adjustment for the clamp glucose variation. CONCLUSION: We conclude that, in lean subjects, insulin inhibits its own secretion, and this may be related to insulin sensibility. This response is blunted in morbidly obese patients and may have a role in the pathogenesis of fasting hyperinsulinemia in these patients.

Reduced renal sodium excretion in primary hypertensive patients after an oral glucose load.

This study was designed to determine urinary sodium excretion in response to an oral glucose load in hypertensive patients. Fifteen hypertensive patients and eighteen normotensive subjects were studied after an overnight fast and for 4 h after the ingestion of 100 g glucose. A subgroup of untreated, nonobese, primary hypertensive patients (five of the 15 hypertensive patients) became hyperinsulinemic (total area under the insulin curve [TAUC]: 33,080 +/- 3348 microU ml(-1) 120 min-1) in response to an oral glucose load compared to normotensive subjects (TAUC: 3670 < 13.731 < 23,693 microU ml(-1) 120 min-1) or to be other subgroup of normoinsulinemic hypertensive individuals TAUC: 10,221 +/- 1615 microU ml-1 120 min-1) despite a similar serum glucose concentration in both groups. A significant decrease in renal sodium excretion in the entire hypertensive group (47.1 +/- 4.7%, P < 0.019) compared to the normotensive (20.0 +/- 10.5%) subjects was also observed during the oral glucose tolerance test. Decreased renal sodium excretion was followed by a transient increase in urinary acid excretion. We speculate that the increase in insulin secretion may be responsible for the sodium-dependent increase in intracellular Ca2+, cellular H+ output and blood pressure in a subgroup of salt-sensitive patients with hypertension. New studies should be designed to identify the precise mechanisms involved in the interaction between hypertension, serum insulin-glucose levels and the magnitude of the renal tubule reabsorption abnormality.

Reduced renal sodium excretion in primary hypertensive patients after an oral glucose load

This study was designed to determine urinary sodium excretion in response to an oral glucose load in hypertensive patients. Fifteen hypertensive patients and eighteen normotensive subjects were studied after an overnight fast and for 4 h after the ingestion of 100 g glucose. A subgroup of intreated, nonobese, primary hypertensive patients (five of the 15 hypertensive patients) became hyperinsulinemic (total area under the insulin curve[TAUC]:33,080 + 3349 muU ml(-1) 120 min(-1) in response to an oral glucose load compared to normotensive subjects (TAUC: 3670<13.731<23,693 muU ml(-1) 120 min(-1) or to the other subgroup of normoinsulinemic hypertensive individuals (TAUC:10,221 + 1615 muU ml(-1) 120 min(-1) despite a similar serum glucose concentration in both groups. A significant decrease in renal sodium excretion in the entire hypertensive group (47.1 + 4.7 per cent, P<0.019) compared to the normotensive (20.0 + 10.5 per cent) subjects was also observed during the oral glucose tolerance test. Decreased renal sodium excretion was followed by a transient increase in urinary acid excretion. We speculate that the increase in insulin secretion may be responsible for the sodium-dependent increase in intracellular Ca2+, cellular H+ output and blood pressure in a subgroup of salt-sensitive patients with hypertension. New studies should be designed to identify the precise mechanisms involved in the interaction between hypertension, serum insulin-glucose levels and the magnitude of the renal tubule reabsorption abnormality.

Heterogenous insulin response to an oral glucose load by patients with the indeterminate clinical form of Chagas' disease.

This study was designed to investigate the behavior of serum glucose and insulin in response to an oral glucose load in chagasic patients with the indeterminate clinical form of the disease. Sixteen chagasic patients and 28 healthy control subjects were studied after an overnight fast and during 2 h after ingestion of 100 g glucose. There were no significant differences in serum glucose levels before and 2 h after the glucose load between chagasic and control subjects. However, in 8 chagasic patients, the total area under the insulin curve was significantly lower (2976 +/- 448 microU ml-1 120 min-1) than in the control (10123 +/- 995 microU ml-1 120 min-1) and in the remaining chagasic patients (9220 +/- 826 microU ml-1 120 min-1). These results suggest that the hypoinsulinemia of this subgroup of chagasic patients may be secondary to reduced insulin secretion and/or to increased peripheral insulin sensitivity probably related to autonomic dysfunction.

Heterogenous insulin response to an oral glucose load by patients with the indeterminate clinical form of Chagas' disease

This study was designed to investigate the behavior of serum glucose and insulin in response to an oral glucose load in chagasic patients with the indeterminate clinical form of the disease. Sixteen chagasic patients and 28 healthy control subjects were studied after an overnight fast and during 2 h after ingestion of 100 g glucose. There were no significant differences in serum glucose levels before and 2 h after the glucose load between chagasic and control subjects. However, in 8 chagasic patients, the total area under the insulin curve was significantly lower (2976 +/- 448 microU ml-1 120 min-1) than in the control (10123 +/- 995 microU ml-1 120 min-1) and in the remaining chagasic patients (9220 +/- 826 microU ml-1 120 min-1). These results suggest that the hypoinsulinemia of this subgroup of chagasic patients may be secondary to reduced insulin secretion and/or to increased peripheral insulin sensitivity probably related to autonomic dysfunction

Insulinemia and blood pressure responses to oral glucose load in primary hypertensive patients.

Fourteen hypertensive patients and 14 normotensive control subjects were submitted to the oral glucose test and their plasma potassium, glucose and insulin levels were measured. Cardiovascular responses were evaluated by blood pressure and pulse rate measurements. Five of 14 hypertensive patients were hyperinsulinemic and had higher blood glucose levels, suggesting insulin resistance. Systolic blood pressure, heart rate and double product increased significantly in normotensive subjects and slightly in hyperinsulinemic patients, but not in normoinsulinemic hypertensive patients. These results seem to indicate the presence of insulin resistance in a particular group of primary hypertensive patients and a smaller cardiovascular response after glucose overload.

Insulin resistance in essential hypertension.

To determine the possible existence of a relationship between insulin resistance and sympathetic nervous system activity in essential hypertension, we calculated the double cross index for 14 hypertensive subjects and 14 normotensive subjects submitted to the oral glucose test. Plasma glucose and insulin levels were similar in hypertensive and normotensive subjects. After glucose loading, however, both parameters were significantly higher in hypertensive subjects. Five out of 14 hypertensive patients were hyperinsulinemic. The increase in double cross index following a glucose load was significantly higher in normotensive volunteers than in hyperinsulinemic hypertensive subjects. No change in double cross index was observed in normoinsulinemic hypertensive subjects. Thus, insulin resistance, high blood glucose level, impairment of cardiac response and hyperinsulinemia are present in a significant portion of hypertensive patients. Hyperinsulinemia may contribute to hypertension by stimulating sympathetic nervous system activity, by influencing the calcium transport across the cell membrane and/or by some other mechanism.

Insulin resistance in essential hypertension

To determine the possible existence of a relationship between insulin resistance and sympthetic nervous system activity in essential hypertension, we calculated the double cross index for 14 hypertensive sujects and 14 normotensive subjects submitted to the oral glucose test. Plasma glucose and insulin levels were similar in hypertensive and normotensive subjects. After glucose loading, however, both parameters were significantly higher in hypertensive subjects. Five out of 14 hypertensive patients were hyperinsulinemic. The increase in double cross index following a glucose load was significantly higher in normotensive volunteers than in hyperinsulinemic hypertensive subjects. No change in double cross index was observed in normoinsulinemic hypertensive subjects. Thus, insulin resistance, high blood glucose level, impairment of cardiac response and hyperinsulinemia are present in a significant portion of hypertensive patients. Hyperinsulinemia may contribute to hypertensión by stimulating sympathetic nervous system activity, by influencing the calcium transport across the cell membrane and/or by some other mechanism

Anticorpos EVI e NP na infeccao chagasica cronica. Estudo em pacientes com diferentes formas clinicas. / EVI and NP antibodies in chronic Chagas' infection.Study in patients with different clinical forms

Para verificar se existe correlacao entre os anticorpos EVI e NP e a infeccao chagasica cronica, foram estudados 56 pacientes sorologicamente positivos para o T. cruzi,que apresentavam diferentes formas clinicas desta infeccao. Foram tambem estudados 75 soros com reacoes negativas para T. cruzi, para determinar os titulos de EVI e NP que nao pertencem a esta populacao. Os resultados demonstram que titulo > ou igual a 1:32 podem ser tomados como positivos tanto para EVI quanto para NP. Considerando este titulo, verificamos que 69,6% e 70,1% dos pacientes chagasicos apresentam anticorpos EVI e NP respectivamente, e somente 3% dos individuos nao infectados apresentavam titulos de 1:32. Estes dados mostram a estreita relacao existente entre EVI, NP, e a infeccao chagasica. Porem, quando se analisou a presenca desses anticorpos em pacientes com as diferentes formas clinicas da doenca, nao foi encontrada diferenca significativa entre os grupos estudados