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Clinical and metabolic data of twenty patients with hyperosmolar nonketotic coma (HNC) and ten patients in ketoacidosis (DA) are compared. HNC patients were older; fewer were previously known diabetics; more had multiple chronic diseases. Common precipitating factors in HNC included infection, dehydration and administration of diabetogenic drugs. Blood glucose and urea nitrogen, plasma sodium, bicarbonate and osmolarity were significantly higher in HNC. Plasma potassium and chloride levels were similar in both groups. Patients with HNC had significantly lower plasma levels of free fatty acids, cortisol and growth hormone.Plasma insulin levels in HNC were low and not significantly different from those observed in KA. Patients with HNC required more fluids and less insulin therapy. Mortality was 20 per cent in HNC, lower than that generally observed in this condition, but higher than that of KA, 0 per cent.On the basis of the above findings, it is suggested that dehydration and hyperosmolarity may play significant roles in the etiology of HNC, and that therapy should, therefore, be directed at restoration of normal osmolarity and correction of water deficits with 0.45 per cent saline and moderate amounts of insulin. DIABETES 20: 228-38, April, 1971. Hyperosmolar nonketotic coma is a syndrome characterized by severe hyperglycemia, hyperosmolarity and dehydration in the absence of ketoacidosis. Although first described by Frerichs 1 more than eighty years ago, this condition received little attention until the report of Sament and Schwartz 2 in 1957. Soon afterward additional reports appeared and by 1965 Schwartz and Apfelbaum 3 were able to review sixty-three cases collected from the world literature. Over two hundred case reports have now been published and available data 4 indicate that this syndrome is approximately one sixth as frequent a cause of coma as ketoacidosis. Despite increased recognition, the published mortality rate remains in the order of 40 per cent

Cells grown in culture from rat islet cell tumor (parent cells) and clones obtained from them were used in this study. Parent cells secreted primarily insulin and somatostatin with very small quantities of glucagon. The clones, based on hormone content and secretion, were divided into three phenotypic groups: insulin secreting, somatostatin secreting, and nonsecreting clones. Specific receptors for insulin, glucagon, and somatostatin were demonstrated on parent cells and clones. Parent cells bound 4.12 +/- 0.46% insulin, 2.11 +/- 0.29% glucagon, and 2.49 +/- 1.24% somatostatin per 2 x 10(6) cells. Characteristic hormone binding patterns were observed in insulin secreting versus somatostatin secreting clones. Insulin secreting versus somatostatin secreting clones. Insulin secreting clones bound less insulin than somatostatin and other noninsulin-secreting clones (P less than 0.02). In contrast, somatostatin secreting clones bound more somatostatin than non-somatostatin-secreting clones (P less than 0.05). Somatostatin-secreting clones had a significantly greater number of receptors for all three hormones. The difficulties involved in the interpretation of the quantitative aspects of binding in the presence of continued hormone secretion are discussed. Nonetheless, the presence of receptors on the cells for hormones secreted by the same cells strongly suggests autoregulation. The apparent low affinity of some of these receptors and the presence of receptors for all three islet cell hormones on all islet cells supports the likelihood of paracrine controls.

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The SHR/N-cp rat is a new genetically obese model for non-insulin-dependent diabetes mellitus. Expression of the diabetes is enhanced by a high-sucrose (54%) diet. After 4 wk on the diet, the cp/cp rats weigh significantly more than their +/? controls, have postprandial hyperglycemia (greater than 400 mg/dl), and are hyperinsulinemic, with immunoreactive insulin (IRI) levels 10- to 20-fold greater than controls. Total pancreatic IRI tends to be increased 1.6-fold in the cp/cp rats (although not significantly). There is no increase in pancreatic proinsulin content as a percent of total IRI. Studies of in vitro pancreatic function were carried out with the isolated nonrecirculating perfused pancreas method. The cp/cp rats (n = 10) showed impaired or absent IRI responses to 16.5 mM glucose, whereas +/? rats (n = 9) responded with classic biphasic curves. Comparison of insulin secreted in 20 min revealed a greater than 53% decrease in IRI secretion in cp/cp rats (P less than .05). A paradoxical hypersecretion of IRI at glucose concentrations of 0-2.7 mM was noted in cp/cp but not lean rats, i.e., 1.8 +/- 0.2 mU/min IRI in cp/cp rats vs. 0.04 +/- 0.007 mU/min in +/? rats. Perfusion of pancreases for 45 min with buffers containing no glucose resulted in restoration of a normal biphasic IRI response to 16.5 mM glucose in the cp/cp rats, whereas response in the lean rats was markedly reduced. Brisk IRI responses to 10 mM arginine in buffers with no glucose also occurred in cp/cp but not +/? rats. Glucagon secretion was relatively suppressed in the cp/cp rats.(ABSTRACT TRUNCATED AT 250 WORDS)