Early administration of the glucose-dependent insulinotropic polypeptide receptor antagonist (Pro(3))GIP prevents the development of diabetes and related metabolic abnormalities associated with genetically inherited obesity in ob/ob mice

Aims/hypothesis Ablation of gastric inhibitory polypeptide ( GIP) receptor action is reported to protect against obesity and associated metabolic abnormalities. The aim of this study was to use prediabetic ob/ob mice to examine whether 60 days of chemical GIP receptor ablation with (Pro(3)) GIP is able to counter the development of genetic obesity-related diabetes.

Recessive congenital methaemoglobinaemia: cytochrome b(5) reductase deficiency

Some 60 years ago, Quentin Gibson reported the first hereditary disorder involving an enzyme when he deduced that familial methaemoglobinaemia was caused by an enzymatic lesion associated with the glycolysis pathway in red blood cells. This disorder, now known as recessive congenital methaemoglobinaemia (RCM), is caused by NADH-cytochrome b5 reductase (cb(5)r) deficiency. Two distinct clinical forms, types I and II, have been recognized, both characterized by cyanosis from birth. In type II, the cyanosis is accompanied by neurological impairment and reduced life expectancy. Cytochrome b(5) reductase is composed of one FAD and one NADH binding domain linked by a hinge region. It is encoded by the CYB5R3 (previously known as DIA1) gene and more than 40 mutations have been described, some of which are common to both types of RCM. Mutations associated with type II tend to cause incorrect splicing, disruption of the active site or truncation of the protein. At present the description of the sequence variants of cb(5)r in the literature is confusing, due to the use of two conventions which differ by one codon position. Herein we propose a new system for nomenclature of cb(5)r based on recommendations of the Human Genome Variation Society. The development of a heterologous expression system has allowed the impact of naturally occurring variants of cb(5)r to be assessed and has provided insight into the function of cb(5)r.

Detecting motor abnormalities in preterm infants

As a consequence of the fragility of various neural structures, preterm infants born at a low gestation and/or birthweight are at an increased risk of developing motor abnormalities. The lack of a reliable means of assessing motor integrity prevents early therapeutic intervention. In this paper, we propose a new method of assessing neonatal motor performance, namely the recording and subsequent analysis of intraoral sucking pressures generated when feeding nutritively. By measuring the infant's control of sucking in terms of a new development of tau theory, normal patterns of intraoral motor control were established for term infants. Using this same measure, the present study revealed irregularities in sucking control of preterm infants. When these findings were compared to a physiotherapist's assessment six months later, the preterm infants who sucked irregularly were found to be delayed in their motor development. Perhaps a goal-directed behaviour such as sucking control that can be measured objectively at a very young age, could be included as part of the neurological assessment of the preterm infant. More accurate classification of a preterm infant's movement abnormalities would allow for early therapeutic interventions to be realised when the infant is still acquiring the most basic of motor functions. (C) Springer-Verlag 2000.

Cardiovascular and metabolic abnormalities in the offspring of diabetic pregnancy

Aims/hypothesis. Maternal fuel metabolism is known to exert long range effects on the later development of children of diabetic mothers. Recently cardiovascular disease in adult life has been linked retrospectively with foetal malnutrition. The aim of this study was to identify whether markers for fuel-related cardiovascular programming exist for the offspring of diabetic pregnancy.