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Objectives Severe hypoglycemia is associated with cognitive decline and dementia in older persons with type 2 diabetes. The role of antidiabetic treatments on severe hypoglycemia is unknown in dementia. The aims were to determine the prevalence of severe hypoglycemic events and investigate associations among severe hypoglycemic and specific antidiabetic treatments (classes of oral agents and types of insulin analogs) in a large sample of nursing home patients with diabetes according to dementia status. Design Cross-sectional observational study. Setting A total of 150 nursing homes across Italy. Participants A total of 2258 patients with type 2 diabetes (dementia = 1138, no dementia = 1120). Measurements Diagnosis of dementia before nursing home admission. Data were collected regarding functional status, glycemic control, antidiabetic treatments, comorbidities, and biochemical and clinical measurements. Logistic regression models with severe hypoglycemia as the dependent variable were used to test associations with antidiabetic agents. Results Patients had a mean age (SD) of 82 (8) years, body mass index (BMI) of 25.4 (4.8), fasting plasma glucose (FPG) of 7.5 (3.0) mmol/L, postprandial glucose (PPG) of 10.3 (3.6) mmol/L, HbA1c of 7.1% (54 mmol/L), and impairments in activities of daily living (ADLs) of 3.7 (2.1). Severe hypoglycemia was more prevalent in patients with dementia (18%) compared with patients without dementia (8%). Patients with dementia were older, showed greater ADL impairments, greater number of comorbidities, lower FPG, and higher PPG compared with those without dementia. Adjusted logistic regression models in patients with dementia showed that rapid- and long-acting insulin analogs were associated with reduced odds ratio (OR) (OR 0.333; 95% confidence interval [CI] 0.184–0.602; OR 0.248, 95% CI 0.070–0.882, respectively), whereas sulphonylureas and combined metformin + sulphonylurea were associated with increased ORs (OR 8.805, 95% CI 4.260–18.201; OR 6.639; 95% CI 3.273–14.710, respectively) of experiencing severe hypoglycemia. No correlations were found in patients without dementia. Conclusion In older nursing home patients with type 2 diabetes, severe hypoglycemia was significantly higher in dementia. Our findings suggest that sulphonylureas should be used with caution, whereas rapid- and long-acting insulin analogs seem safer.

L-diabetes represents a subtype of non-autoimmunopathic and non-adipose diabetes mellitus. It is hypothesized that ATP-sensory brain centres measure the cerebral ATP concentration and announce a hypoglycaemia if the setpoint is undercut. The disease involves a decreased ATP formation in the CNS that is independent of blood glucose levels, and that leads to a "hypoglycaemia" false alarm. UGT1-polymorphisms, a sensitive sympathetic system, an IgM deficit and an increased porousity of the mucous membrane of the small intestine have been postulated in its etiology. These causative factors bring about increasing amounts of toxins and radicals which impair the ATP generation in the CNS so that through the announcement of a non-existing hypoglycaemia the release of the insulin antagonists hGH, cortisol and adrenaline is induced.

The work in the author's laboratory is funded by a grant from the Medical Research Council of Canada. The author thanks Susanne Bordeleau-Chenier for excellent secretarial assistance.

SUMMARY Using the effect of insulin on isolated rat hemidiaphragm as an assay system, it has been possible to demonstrate a circulating insulin antagonist in some new cases of diabetes of the growth-onset type as well as during the exacerbation of diabetes secondary to infections. Three out of four acromegalics with diabetes also showed evidence of insulin antagonist, while one diabetic patient with thyrotoxicosis requiring 155 u. insulin/day had no antagonist. The antagonist present in the new diabetics and during infection exhibited some characteristics similar to the antagonist previously described during diabetic acidosis [Field & Stetten, 1956a], but different from the insulin inhibitor present during chronic insulin resistance.

Albumin prepared from serum of diabetic patients inhibits the effect of insulin on rat diaphragm muscle but not on their epididymal fat pads when injected intravenously to make a foreign protein concentration of 3.8 g/100 ml in the plasma of the rat. At this concentration, albumin from normal subjects had no insulin inhibitory effect on either tissue. — These observations confirm, underin vivo conditions, that diabetic albumin is more antagonistic to insulin than albumin prepared from normal subjects.

SummaryThe administration of testosterone propionate in doses of 10, 25, or 50 mg daily for a period of 10 days to 13 patients with diabetes mellitus failed to alter significantly the responsiveness to insulin in all but one. It is suggested that the presence of the side-chain attached to carbon atom 17 in the steroid molecule may be essential for this activity.

The enzyme glutathione-insulin transhydrogenase, that catalyzes sulfhydryldisulfide interchange, inactivates both insulin and proinsulin; the inactivation of insulin takes place at a greater rate than that of proinsulin. Under the experimental conditions used, the enzyme reactivates scrambled proinsulin but does not reactivate scrambled insulin. However, in the presence of connecting peptide of proinsulin reactivation of scrambled insulin is observed, indicating that for the generation of immunoreactive insulin covalent binding of C-peptide is not necessary and residues 31, 32, 59, and 60 of proinsulin may be omitted.

Five siblings had congenital generalized lipodystrophy and systemic cystic angiomatosis. Manifestations of each disease and a suggested mechanism of cause related to rapid mobilization of ...

Patients with essential diabetes including prediabetes have more synalbumin antagonism to insulin than normal subjects or patients with “pancreatic” diabetes, e.g. after pancreatectomy. Thus excessive synalbumin antagonism (synalbumin positive) can be regarded as a biochemical marker to ascertain whether a given person is constituted as an essential diabetic-without reference to carbohydrate intolerance.-On this premise, the genetic transmission of essential diabetes has been examined by studying the relatives of essential diabetics. The results strongly suggest that excessive synalbumin antagonism is inherited as an autosomal “dominant” character.-Ninety-seven members of nine families were studied, 39 were synalbumin negative whereas 58 were synalbumin positive, but only 16 of these latter have overt carbohydrate intolerance. A further three have spontaneous hypoglycaemia whereas the remainder are quite asymptomatic. These observations suggest that overt carbohydrate intolerance is relatively uncommon or will be a late event in many people constituted as essential diabetics.

DURING the investigation of the insulin antagonism associated with human serum albumin1, ‘Visking’ tubing (Visking Corporation, Chicago, U.S.A,) was used for ultrafiltration and dialysis of protein solutions. The tubing itself has since been found to give rise to a substance which antagonizes insulin and which appears in the following circumstances: (1) When distilled water is ultrafiltered through 7-ft. of heavy grade ‘Visking’ tubing (27/32 in. inflated diameter) supported by ‘Terylene’ net, under a negative pressure of 40–50 cm. mercury, over a period of three days. (2) When 7 ft. light grade ‘Visking’ tubing (18/32 in.) is filled with water and suspended in changes of distilled water for 2–7 days, that is, used as dialysis tubing.

Da Guanidinosuccinsaure in der Uramie akkumuliert, wurde angenommen, dass dieses Stoffwechselprodukt bei Niereninsuffizienz die bekannte Glukoseintoleranz verursachen konnte. In-vitro-Versuche am Rattenzwerchfell haben diese Hypothese jedoch nicht bestatigen konnen, da Guanidinosuccinsaure in der Konzentration von 3 mg/100 ml keinen Einfluss auf die basale oder insulinstimulierte Glucoseaufnahme durch dieses Gewebe zeigte.