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Obesity is characterised by alterations in metabolic function which result from a combination of increasing total body fatness and the regional distribution of adipose tissue. Abdominal visceral obesity is particularly associated with hyperinsulinaemia, increased portal vein free fatty acid concentration, hepatic gluconeogenesis, altered adrenocortical activity and androgen secretion and reduced plasma sex hormone binding globulin levels. These alterations, which are accompanied by changes in visceral adipocyte sensitivity to plasma catecholamine stimulation, enhance further visceral fat deposition and the perpetuation of the metabolic derangements. The characteristic dyslipidaemia associated with upper body obesity and the frequent development of NIDDM are predictable consequences. In contrast to the considerable knowledge about the biochemical background to these alterations, relatively little is understood about the mechanisms through which an individual's ethnic background influences the changes. This chapter reviews these important issues.

Obesity frequently clusters with hypertension, hyperlipidemia, non-insulin-dependent diabetes mellitus, and ischemic heart disease with hyperinsulinemia as syndrome X. Although central obesity has been recognized to have a strong genetic component, few candidate genes have been studied in this disorder. After a recently described association between the apolipoprotein-D (Apo-D) gene polymorphism and non-insulin-dependent diabetes mellitus by our group, we have now looked at a TaqI polymorphism of the Apo-D gene in two other components of syndrome X, namely obesity and hyperinsulinemia. Apo-D genotype differences were found between obese subjects (n = 57) and slim controls (n = 57; P = 0.006). Furthermore, in the obese group an association was found between the Apo-D genotype and fasting insulin (P < 0.001). Preliminary evidence, therefore, suggests that the TaqI Apo-D polymorphism can be used as a genetic marker for obesity and several components of syndrome X.

Somatostatin has been shown to be effective in the management of the dumping syndrome and there have been reports of the effective use of long acting somatostatin analogue in the management of this condition. However, there have been few reports of the prolonged use of a somatostatin analogue in the late dumping syndrome. We describe a patient in whom this management provided good long term symptomatic relief which was confirmed biochemically.

A study of intravenous (i.v.) cannula usage for medical emergencies admitted to hospitals in the Newham Health District was undertaken during two defined periods (24 and 35 days). Almost half the cannulas inserted (47%) were not flushed following an initial bolus injection of heparinized saline. The duration that cannulas remained in a vein ranged from 24 hours to 8 days (median 2 days) and inflammation around the cannula site was related to the length of time since insertion but unrelated to whether the cannula was flushed regularly or to the type of fluid used. Our findings indicate a substantial wastage of i.v. cannulas due to difficulties with insertion and suggest that isotonic saline, without heparin, is effective in maintaining cannula patency for 48 hours. It is concluded that these findings are not unique to the Newham Health District and worthwhile financial savings should be achieved throughout the NHS if clinicians reconsider the indications and use of i.v. cannulas for their patients.