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""Congenitally analbuminaemic individuals and rats (NARs) exhibit several metabolic abnormalities, including hypertriglyceridaemia and plasma free fatty acid deficiency. Our aim was to study glucose homeostasis and insulin secretion in NARs. Plasma concentrations of lipids, glucose and insulin and secretion of insulin from the pancreatic islets were measured in female NARs and control animals (Sprague�CDawley rats; SDRs). Glucose homeostasis tests were also performed. Plasma glucose levels were similar between NARs and SDRs, irrespective of feeding status. However, fed insulinaemia [http://www.selleckchem.com/products/Nutlin-3.html Nutlin-3 in vitro] was ?37% higher (P�� 0.05) in NARs than in SDRs. The NARs displayed a markedly increased glucose tolerance, i.e. the integrated glycaemic response was one-third [http://en.wikipedia.org/wiki/INPP5D INPP5D] that of the control animals. Enhanced glucose tolerance was associated with threefold higher insulinaemia at peak glycaemia after a glucose load than in the control animals. Similar peripheral insulin sensitivity was observed between groups. Isolated pancreatic islets from NARs secreted significantly more insulin than islets from SDRs in response to a wide range of glucose concentrations (2.8�C33.3 mm). Despite having similar liver glycogen contents in the fully fed state, NARs had ?40% (P�� 0.05) lower glycogen contents than SDRs after 6 h fasting. The injection of a gluconeogenic substrate, pyruvate, elicited a faster rise in glycaemia in NARs compared with SDRs. Overall, NARs displayed enhanced glucose tolerance, insulin secretion and gluconeogenic flux. The higher glucose tolerance in NARs compared with SDRs is attributed to enhanced islet responsiveness to secretagogues, while peripheral insulin sensitivity seems not to be involved in this alteration. We propose that the enhanced glucose metabolism is a chronic compensatory adaptation to decreased free fatty acid availability in NARs. Congenital analbuminaemia is a rare autosomal recessive disorder characterized by very low levels of plasma albumin ([http://www.selleckchem.com/products/RO4929097.html RO4929097] and intestinal protein loss (Weinstock et al. 1979). This abnormality results from negligible hepatic albumin production due to mutations in the albumin gene (Minchiotti et al. 2008). The first case of human analbuminaemia was reported in 1954 (Kallee, 1996), and several additional cases of human analbuminaemia have been identified. By selectively breeding spontaneously hyperlipidaemic Sprague�CDawley rats (SDRs), Nagase et al. (1979) established a colony of rats, Nagase analbuminaemic rats (NARs), that were confirmed to be analbuminaemic. These rats model many features of human familial analbuminaemia (Baldo-Enzi et al. 1987).