RESUMEN
Although diet therapy is considered the cornerstone of therapy for obese patients with non-insulin-dependent diabetes mellitus, losing weight is often difficult, and the plasma glucose concentration does not always improve after weight loss. We looked for predictors of improvement in plasma glucose levels after weight loss in 135 obese patients with non-insulin-dependent diabetes mellitus who had lost at least 9.1 kg of body weight. After weight loss there was a bimodal distribution of plasma glucose levels, allowing us to identify patients as "responders" or "nonresponders" according to whether a random plasma glucose level was above or below 10.0 mmol/L after a 9.1-kg weight loss. Fifty-five (41%) of 135 patients were responders (after a 9.1-kg weight loss, the mean +/- SEM plasma glucose level was 7.0 +/- 0.2 mmol/L). Many responders had improved plasma glucose levels after only slight weight loss. Eighty (59%) of 135 patients were nonresponders (after a 9.1-kg weight loss, the mean +/- SEM plasma glucose level was 18.3 +/- 0.6 mmol/L). Although the responder and nonresponder groups were comparable in age, sex distribution, plasma glucose levels, and body weight at initial presentation, improvement in the plasma glucose level after weight loss could be predicted by a plasma glucose level of 10.0 mmol/L or lower after 2.3-kg (62% positive predictive value) and 4.5-kg (79% positive predictive value) weight loss. We conclude that, in contrast to conventional teaching, many patients with non-insulin-dependent diabetes mellitus will not have any improvement in plasma glucose levels after a 9.1-kg weight loss. However, a substantial minority (approximately 40%) of obese patients with non-insulin-dependent diabetes mellitus have much lower plasma glucose levels with a weight loss of 9.1 kg or less. Although the plasma glucose response to weight loss cannot be forecast by initial clinical parameters, the success or failure of diet therapy can be predicted from the plasma glucose level after a weight loss of only 2.3 to 4.5 kg. Mild or moderately obese patients with non-insulin-dependent diabetes mellitus who remain hyperglycemic after a weight loss of 2.3 to 9.1 kg are unlikely to improve with further weight loss and should be considered for treatment with insulin or oral hypoglycemic agents.
Asunto(s)
Glucemia/metabolismo , Diabetes Mellitus Tipo 2/dietoterapia , Diabetes Mellitus/dietoterapia , Dieta Reductora , Obesidad , Diabetes Mellitus/sangre , Diabetes Mellitus Tipo 2/sangre , Femenino , Estudios de Seguimiento , Humanos , Masculino , Persona de Mediana Edad , Factores de Tiempo , Pérdida de PesoRESUMEN
Evidence now exists that maintaining normal maternal plasma glucose in the diabetic mother results in an infant mortality risk equal to that in the general population and may reduce the late fetal complications of maternal diabetes: macrosomia and perinatal hypoglycemia. Careful attention to diet, home glucose monitoring, multiple insulin injections, and frequent dose adjustments are often required to achieve this goal. Since organ development occurs within the first few weeks after conception, pregnancy planning and optimization of diabetes management prior to pregnancy is critical to good outcome in diabetic women eager to begin a family.
Asunto(s)
Embarazo en Diabéticas/terapia , Femenino , Feto/fisiología , Humanos , Embarazo , Embarazo en Diabéticas/diagnósticoRESUMEN
Established urodynamic and electrophysiological techniques have been applied to assess the frequency and extent of autonomic and peripheral neuropathy in 60 subjects with diabetes mellitus; 38 were diabetics with suggestive symptoms and the others were representative newly diagnosed (11) or treated (11) diabetics. Objective evidence neuropathic bladder dysfunction was detected in 43 of them (71.7%). The commonest abnormality was a hypotonic, insensitive large capacity bladder, which condition was usually asymptomatic. Less freuqently (15%) was this complicated by bladder decompensation and sphincter involvement, resulting in excessive residual urine and infection; some of these had bladder paralysis with chronic painless retention of urine (7%). Electrophysiological studies found a sensory defect in the lower limbs in all tested patients (100%), and in 41 patients (69%) as associated motor conduction abnormality, which was more frequent and marked in the lower than the upper limb. These functional abnormalities appeared to be related to the severity of diabetes, but less to its duration. Indeed of 11 newly diagnosed diabetics tested 7 had a peripheral neuropathy and 4 urodynamic abnormalities. The high incidence of bladder dysfunction and peripheral neuropathy in this series indicates the frequency of subclinical diabetic neuropathy and a factor needing more emphasis in diabetic uropathy.
Asunto(s)
Neuropatías Diabéticas/fisiopatología , Vejiga Urinaria Neurogénica/fisiopatología , Adulto , Anciano , Neuropatías Diabéticas/complicaciones , Disfunción Eréctil/etiología , Femenino , Humanos , Masculino , Neuronas Motoras/fisiología , Conducción Nerviosa , Neuronas Aferentes/fisiología , Vejiga Urinaria Neurogénica/etiología , Orina/fisiologíaRESUMEN
Serum-lipid concentrations and their relationship to blood-glucose and serum-insulin were examined in non-insulin-requiring diabetics, 62 with and 45 without retinopathy. The age, sex-body-weight, and duration of known diabetes was comparable in the two groups. All were treated by diet only or diet and oral hypoglycaemic agents. Patients with retinopathy had higher fasting serumtriglyceride and serum--cholesterol levels than those without. Compared with a non-diabetic population, significantly more diabetics with retinopathy had raised derum-lipids. The lipid concentrations did not correlate with body-weight, serum-thyroid-stimulating-hormone levels, renal involvement, or fasting blood-sugar. While the blood-sugar concentrations were similiar in the two groups the absolute insulin increment and the relative insulin response to a 50 g. oral glucose load were significantly lower in those with retinopathy than in those without. The impairment of insulin response correlated significantly with the frequency of hyperlipidaemia. It is suggested that insulin deficiency with secondary hyperlipidaemia is characteristic of diabetic patients with retinopathy.