RESUMEN
A whey protein/guar gum preload reduces postprandial glycaemia in type 2 diabetes through slowing gastric emptying. However, gastric emptying has previously been assessed using a stable isotope breath test technique, which cannot discriminate between slowing of gastric emptying and small intestinal absorption. This preload also may be useful in the management of postprandial hypotension. We evaluated the effects of a whey protein/guar preload on gastric emptying, glucose absorption, glycaemic/insulinaemic and blood pressure (BP) responses to an oral glucose load. Eighteen healthy older participants underwent measurements of gastric emptying (scintigraphy), plasma glucose and insulin, glucose absorption, superior mesenteric artery (SMA) flow, BP and heart rate (HR) after ingesting a 50 g glucose drink, with or without the preload. The preload reduced plasma glucose (p = 0.02) and serum 3-O-methylglucose (3-OMG) (p = 0.003), and increased plasma insulin (p = 0.03). There was no difference in gastric emptying or BP between the two days. The reduction in plasma glucose on the preload day was related to the reduction in glucose absorption (r = 0.71, p = 0.002). In conclusion, the glucose-lowering effect of the preload may relate to delayed small intestinal glucose absorption and insulin stimulation, rather than slowing of gastric emptying.
Asunto(s)
Glucemia/efectos de los fármacos , Presión Sanguínea/efectos de los fármacos , Galactanos/farmacología , Vaciamiento Gástrico/efectos de los fármacos , Absorción Intestinal/efectos de los fármacos , Mananos/farmacología , Gomas de Plantas/farmacología , Proteína de Suero de Leche/farmacología , 3-O-Metilglucosa/sangre , Anciano , Femenino , Voluntarios Sanos , Frecuencia Cardíaca/efectos de los fármacos , Humanos , Insulina/sangre , Intestino Delgado/metabolismo , Masculino , Periodo Posprandial/efectos de los fármacosRESUMEN
The role of TNF and its type 1 receptor (TNFR1) in the pathogenesis of collagen-induced arthritis (CIA) was investigated in mice using two approaches. First, DBA/1 mice were treated after immunization with type II collagen by injecting TNFR1-IgG1 fusion protein to neutralize systemic TNF. CIA was prevented when treatment was administered shortly before the onset of clinical disease, suggesting that TNF is a crucial mediator in the late initiation phase of the arthritic process. In a second approach, TNFR1-deficient mice, generated by gene targeting and crossed to DBA/1, were used. These mice developed CIA with a low incidence and in a milder form. However, once a joint was afflicted, the disease progressed in this joint to the same end stage as that in wild-type mice. These data suggest that TNFR1 is the main transducer of TNF proinflammatory effects establishing CIA, but the progression of arthritis to tissue destruction and ankylosis is independent of TNFR1.
Asunto(s)
Antígenos CD/fisiología , Artritis/prevención & control , Colágeno/inmunología , Inmunización Pasiva , Inmunoglobulina G/farmacología , Cadenas Pesadas de Inmunoglobulina/metabolismo , Receptores del Factor de Necrosis Tumoral/metabolismo , Receptores del Factor de Necrosis Tumoral/fisiología , Factor de Necrosis Tumoral alfa/fisiología , Animales , Antígenos CD/química , Antígenos CD/genética , Antígenos CD/metabolismo , Artritis/etiología , Artritis/inmunología , Artritis/patología , Artritis Reumatoide , Secuencia de Bases , Quimera , Cruzamientos Genéticos , Modelos Animales de Enfermedad , Progresión de la Enfermedad , Susceptibilidad a Enfermedades , Marcación de Gen , Inmunización , Inmunoglobulina G/inmunología , Cadenas Pesadas de Inmunoglobulina/inmunología , Cadenas gamma de Inmunoglobulina , Ratones , Ratones Endogámicos C57BL , Ratones Endogámicos DBA , Ratones Noqueados , Datos de Secuencia Molecular , Receptores del Factor de Necrosis Tumoral/química , Receptores del Factor de Necrosis Tumoral/genética , Receptores del Factor de Necrosis Tumoral/inmunología , Receptores Tipo I de Factores de Necrosis Tumoral , Proteínas Recombinantes de Fusión/inmunología , Proteínas Recombinantes de Fusión/metabolismoRESUMEN
In familial Bartter's syndrome, hyperprostaglandinuria is considered a constant feature and prostanoid synthetase inhibition often positively influences the disease course. The urinary calcium excretion distinguishes two clinically and biochemically different variants, namely, classic Bartter's syndrome (normocalciuric or hypercalciuric variant; urinary calcium to creatinine > or = 35.3 mg/mg 10(-3)) and Gitelman's syndrome (hypocalciuric variant; urinary calcium to creatinine < 35.3 mg/mg 10(-3)). In the hypocalciuric variant of Bartter's syndrome prostanoid synthetase inhibition is of little benefit. Since the production of prostanoids has not been extensively studied in Gitelman's syndrome, the urinary excretion of prostaglandin E2 was assessed by radioimmunoassay in 11 untreated patients with Gitelman's syndrome (aged 10 to 21 years; five females and six males) and in 11 healthy controls (aged 11 to 20 years; five females and six males). The urinary excretion of prostaglandin E2 was similar in both study groups. The study provides the rationale for the poor effect of prostanoid synthetase inhibition in the hypocalciuric variant of Bartter's syndrome. The assessment of urinary excretion of prostaglandin E2 does not represent a diagnostic sine qua non in the context of familial Bartter's syndrome.
Asunto(s)
Síndrome de Bartter/orina , Calcio/orina , Dinoprostona/orina , Adolescente , Adulto , Síndrome de Bartter/diagnóstico , Síndrome de Bartter/genética , Estudios de Casos y Controles , Niño , Diagnóstico Diferencial , Femenino , Humanos , Masculino , Radioinmunoensayo , SíndromeRESUMEN
BACKGROUND: The anatomy of the orbital arteries is well known, and their physiology is under intensive investigation. Their age-related or other pathologic alterations, however, are still largely unknown. METHOD: We obtained at autopsy 16 orbits from 8 persons aged > 70 years, and 4 orbits from 2 persons between 40 and 50 years. Specimens were taken from 20 locations along the orbital arteries, from the internal carotid to the globe, and studied by light microscopy. RESULTS: We observed the following arteriosclerotic changes, in order of decreasing frequency: intimal hyperplasia, medial atrophy, atherosclerotic fibrous plaques, and calcifications of the internal elastic lamina. The frequency and severity generally decreased with smaller arterial caliber. CONCLUSION: Arteriosclerosis was ubiquitous in persons > 70 years of age. Degenerative changes in aged human orbital arteries may play an important role in ophthalmic vascular diseases.