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The autologous-serum skin test (ASST) can cause a wheal-and-flare response in some cases of chronic idiopathic urticaria. We subjected 102 patients affected by chronic idiopathic urticaria to this test and studied some clinical parameters to detect any significant differences between ASST-positive and ASST-negative patients. The only significant difference we noted between the two groups was the incidence of angioedema (P = 0.01). We suggest that the ASST cannot be used alone either to predict the severity of urticaria or to define it as 'autoimmune'.

The study was performed on 289 female patients (aged 20-60) of a family doctor in Castel D'Azzano, a small town near Verona. The following variables were considered: body mass index (BMI), tricepital, subscapular, hypomesogastric, epimesogastric, supra-iliacal and epitrochanteric skinfolds, waist, umbilical and bitrochanteric circumferences, cholesterol, triglycerides, HDL-cholesterol, glycemia, uricemia and blood pressure. A significant worsening with age was observed in the mean values of the variables. This worsening was particularly evident in women over 50. The population was subdivided according to presence or absence of menopause; the two groups were then matched for age. None of the variables showed significant differences. Our results did not confirm any of the many effects that menopause is supposed to have regarding metabolic and blood pressure alterations.

Insulin binding to human adipose tissue from surgical patients was determined after three different preincubation conditions: a) 24 hrs in the presence or absence of 80 ng/ml insulin; b) 24 hrs in the presence of 80 ng/ml insulin or insulin plus 4 micrograms/ml metformin; c) 48 hrs pre-incubation as in b). We found that insulin down regulated its own receptor after 24 hours pre-incubation; when metformin was present in the pre-incubation medium together with insulin, insulin binding to adipose tissue was significantly higher than in tissue exposed to insulin alone after 48 hrs pre-incubation; a similar effect of metformin was already seen after 24 hrs, but was not statistically significant. We suggest that metformin can correct down regulation of the insulin receptor. This finding could explain discrepant results among studies dealing with the influence of metformin on insulin binding. Moreover, these results could be useful in understanding the mechanism of action of metformin in insulin-resistant states, e.g. type II diabetes.

Starvation causes insulin resistance which is partly due to decrease of insulin action on glucose transport in target cells. Preliminary data from other authors suggest that starvation is associated with an increase of the time necessary for insulin to exert its maximum effect on glucose transport. In order to verify this finding, 3-O-methylglucose (3OMG) transport was studied in isolated rat adipocytes from starved and fed rats. The total intracellular space for 3OMG was not modified by 48h starvation. After 48h starvation, 3OMG transport into fat cells was less responsive to maximum insulin concentration than in controls: 33 +/- 2% (controls) vs 23 +/- 4% (starved) of total glucose space, p less than 0.05; the sensitivity to insulin was normal or even increased in comparison to controls: 50% of maximum effect was reached at 42 microU/ml insulin in controls and at 26 microU/ml insulin in starved animals. We could not find any effect of starvation on the time-response curves of insulin action.