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The fasting blood glucose was studied in 406 patients with carpal tunnel syndrome. We found 3.3% patients with diabetes mellitus and 15% with abnormal blood glucose levels. A prospective study was performed in 36 patients (oral glucose tolerance test, and blood lipid parameters). 45% of the patients in this group had an abnormal OGTT and 52% presented with hyperlipoproteinemia.

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Idiopathic bullae occurring in diabetics constitute an uncommon condition which may reveal the diabetes, announce its decompensation or represent a mere epiphenomenon. The authors report the case of a woman who experienced two episodes of idiopathic bullae: the first one disclosed the diabetes, the second one heralded its decompensation. Both episodes were preceded by painful paraesthesia. The bullae contained a clear and serous fluid and the separation was intradermal. Direct immunofluorescence with anti-fibrin serum only showed fluorescence in the lumen of the bulla and in subjacent dermal areas. Electron microscopy demonstrated that the tissue separation was at the base of the stratum corneum. Other clinical cases and pathogenetic theories found in the literature are reported. In contrast with other bullous diseases occurring in diabetics and often of poor prognosis, idiopathic bullae is a benign condition requiring no more than a symptomatic treatment.

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We have studied liver biopsies obtained in 12 hyperlipoproteinemic (HLP) patients (type II, 6; type IV, 6) treated with diet and fenofibrate, and in 15 patients (type II, 11; type IV, 4) receiving diet only. Electron microscopy of liver biopsies and the morphometric analysis according to the method of Weibel and Rohr showed mitrochondrial changes in patients treated with fenofibrate, these changes depending on the type of hyperlipoproteinemia. In type II HLP, we found a decreased volume of normal mitochondria (fenofibrate, 125.72 +/- 17.04 X 10(-3) cm3/cm3; diet only, 185.84 +/- 8.96 10(-3), P less than .05). In type IV HLP we found a decreased number of giant mitochondria (fenofibrate, 0.08 +/- 0.03 X 10(10) cm-3; diet only, 0.32 +/- 0.08 X 10(10) cm-3, P less than .05) and a decreased volume of altered mitochondria (fenofibrate, 6.00 +/- 1.44 X 10(-3) cm3/cm3; diet only, 13.61 +/- 1.17 X 10(-3), P less than .05). In contrast with the rodent studies, the present study shows no change in the number of volume of peroxisomes.

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Mercury strain gauge venous occlusion plethysmography is a non invasive exploration of the lower limb venous hemodynamic. Classically, venous distensibility (delta V/V %) is expressed in terms of time during venous inflow (venous occlusion) and venous outflow (after cuff deflation). The authors proposed to express the total flow Q of the limb (obtained by a differentiator of the electric signal of the strain gauge) in terms of the venous distensibility (delta V/V %) whatever recording a top each second. This new representation Q = f(delta V/V) permit a more acute visualisation of the initial part of the venous emptying: more differentiation between venous drainage and systolic arterial waves, acceleration then deceleration of the venous emptying, return of the venous wall to its initial position later than venous emptying, active venous constriction. Some parameters are proposed to described this curve and the values obtained in 50 patients without and 10 patients with deep venous thrombosis are reported.

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A morphometric study on liver biopsies from patients with primary hyperlipoproteinemia (IIa n = 4, IIb n = 7, IV n = 7) and in controls (n = 7) was performed by light and electron microscopy. We found hypertrophy of peroxisomes in all subjects with hyperlipoproteinemia. As none of our patients had been given lipid-lowering drugs, this increase in volume seems to be due to hyperlipoproteinemia. Hypertrophy of peroxisomes in hyperlipoproteinemia may constitute a response of the hepatocyte to a disturbed metabolic state. Alterations of peroxisomes in hyperlipoproteinemia may thus occur prior to any lipid-lowering therapy.

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We obtained liver biopsies in 4 patients with type IIA and 7 patients with type IIB hyperlipoproteinemia, and also in 7 healthy controls. A morphometric analysis of liver tissue was carried out by light and electron microscopy. Structural alterations of the hepatocyte and its organelles in type IIA and IIB hyperlipoproteinemia seem to fall into different categories: smaller nuclei, enlarged peroxisomes and altered mitochondria are found in both types of hyperlipoproteinemia, while an increase in the volume of hepatocytes is found only in type IIA. The enlargement of liver peroxisomes in untreated hyperlipoproteinemia is noteworthy, since it has been considered as a marker of the liver toxicity of lipid-lowering drugs.

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The long-term effect of the addition of 20 g wheat bran to the diet is studied over 7 weeks in 4 healthy subjects. No change is found in plasma cholesterol and triacylglycerol. In this experimental design, we find no modification in the plasma levels of the various lipoproteins, except for VLDL cholesterol, which remains significantly lower after 7 weeks of wheat bran ingestion.

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Responses of gastric inhibitory polypeptide (GIP), gastrin and vasoactive intestinal polypeptide (VIP) to a test meal and also nutrient absorption were measured in five healthy men before and after 1, 3 and 7 weeks of daily ingestion of 20 g of wheat bran added to a normal balanced diet. Basal levels of the three hormones were not affected by bran ingestion. Bran ingestion induced a progressive decrease of GIP response to the test meal which became significant after 7 weeks at 30 min (373.9 +/- 71.4 vs 231.1 +/- 47.8 pg/ml, mean +/- s.e.m., P less than 0.05) and at 180 min (389.4 +/- 43.9 vs 262.2 +/- 37.9 pg/ml, P less than 0.01). Gastrin release did not change except for a slight but not significant decrease after 3 weeks. There was no VIP secretion after meal ingestion and addition of bran caused no change. Blood glucose response decreased with time with the greatest effects during the third week with fibre at 30 min (5.00 +/- 0.50 vs 7.38 +/- 0.05 mmol/l before bran), and at 60 min (3.88 +/- 0.34 vs 5.94 +/- 0.27 mmol/l before bran, P less than 0.05). Wet and dry weight of faeces increased by at least 60 per cent from the first week with bran onwards. Faecal nitrogen and fat also increased from 1.77 +/- 0.16 to 2.44 +/- 0.13 g/d for nitrogen (P less than 0.02) and threefold for fat (from 3.78 +/- 0.58 to 10.35 +/- 0.67 per cent dry weight, P less than 0.005) at the third week. Fat and nitrogen contents remained higher until the end of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

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The long-term effect (7 wk) of the addition in the diet of 20 g of wheat bran was studied in five healthy subjects. Blood glucose and plasma insulin were assayed during test-meals taking place before (I), then 10 days (II), 24 days (III), and 45 days (IV) after daily ingestion of wheat bran. Bran addition leads to a time progressive reduction of meal-induced glucose response. This effect was the strongest during meal III, at 30 min (from 7.38 +/- 0.11 to 5.0 +/- 1.11 mmol/l; p less than 0.05) and at 60 min (from 5.94 +/- 0.61 to 3.88 +/- 0.78 mmol/l; p less than 0.05). Insulin response remained identical during the first three test meals. It increased then in a significant manner during meal IV, at 60 min (From 45.5 +/- 12.3 to 61.8 +/- 8.9 microU/ml; p less than 0.02), and at 120 min (from 41.2 +/- 16.3 to 61.0 +/- 16.0 microU/ml; p less than 0.05). The causes of the reduction of glucose response could be potential gastric emptying and intestinal transit increases. The exact mechanism of the improved long-term glucose tolerance seen in brain is not obvious nor is the reason for the enhanced insulin response seen later.

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Blood glucose, gastric inhibitory polypeptide (GIP), vasoactive intestinal polypeptide (VIP) and gastrin secretions were measured over a three-hour period following the ingestion by normal subjects of a mixed meal with two different caloric levels (1055 Kcal and 1192 Kcal). No VIP secretion was observed after either meal. Gastrin release was not modified by the increase of caloric intake (mainly carbohydrates and lipids), whereas GIP secretion was significantly more important after the meal with the highest caloric value (peak at 30 mm: 499.5 +/- 250.4 vs. 273.4 +/- 128.7 pg/ml and integrated response 53.3 +/- 20.5 vs. 28.2 +/- 9.9 ng X ml-1 X 180 min-1-p less than 0.05). This difference could not be attributed to glucose since the blood glucose levels were not significantly different. It is more probably related to the total amount of ingested food. This suggests the existence of rapid mechanisms of adaptation to the incoming load of the GIP-producing cells.

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In rodents fenofibrate shares with other triglyceride-lowering agents the potential to increase the liver peroxisome population. It was therefore of interest to look for this effect in hyperlipoproteinemic patients receiving this drug. Light and electron microscopy of liver biopsies from a group of 10 patients treated with fenofibrate and from another group of 13 receiving diet only, show no morphological difference between both groups. In contrast with the rodent data the morphometric study reveals no significant changes in the number (fenofibrate group: 7.96 10(10) cm-3; group receiving diet alone: 8.41 10(10) peroxisomes per cm3 of liver tissue) or in the size (fenofibrate group: diameter = 0.53 +/- 0.07 micron; group receiving diet alone: 0.50 +/- 0.06) of peroxisomes. The difference between our results and those obtained consistently in rodents may be due to the relatively low dose in man and/or a species-dependant difference in enzyme content of liver peroxisomes, itself related to an apparent difference in the way in which lipids are handled.

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Early lesions of the exocrine pancreas of the Syrian Golden Hamster induced by lifetime weekly oral or subcutaneous administration of N-nitroso-bis (2 hydroxy propyl) amine (250 mg/kg) were studied by light and electron microscopy and autoradiography. There were no pathological differences according to the way of administration. The histogenesis of induced pancreatic neoplasms may be summed up as follows: hyperplasia of ductular cells with new islet cell formation that lead to the development of peri or intra insular cystic ductules which become cystedenomas and carcinomas.

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In rodents fenofibrate shares with other triglyceride-lowering agents the potential to increase the liver peroxisome population. It was therefore of interest to look for this effect in hyperlipoproteinemic patients receiving this drug. Light and electron microscopy of liver biopsies from a group of 10 patients treated with fenofibrate and from another group of 15 receiving diet only, show no morphological difference between both groups. In contrast with the rodent data the morphometric study reveals no significant changes in the number (fenofibrate group: 7.96 10(10) cm-3; group receiving diet alone: 8.41 10(10) peroxisomes/cm3 of liver tissue) or in the size (fenofibrate group: Diameter = 0.53 +/- 0.07 micrometer--group receiving diet alone: 0.50 +/- 0.06) of peroxisomes. The difference between our results and those obtained consistently in rodents may be due to the relatively low dose in man and/or a species-dependent difference in enzyme content of liver peroxisomes, itself related to an apparent difference in the way in which lipids are handled.

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We studied the histological structure of the livers of 36 patients presenting type IV primary hyperlipoproteinaemia. Electron microscopy revealed dilation of the smooth endoplasmic reticulum and rough endoplasmic reticulum as well as the presence of giant mitochondria containing para-crystalline inclusions. Steatosis was present in all type IV hyperlipoproteinaemic patients regardless of their weight or nutritional sensitivity (to alcohol or carbohydrate). The ultrastructural modifications observed by electron microscopy indicate an increased synthesis of very-low-density lipoproteins by the hepatocytes. An alteration in excretion cannot be ruled out with certainty even though the microfilamentary microtubular system was intact, since the qualitative and functional modifications in this system may be undetectable by electron microscopy.

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