Yves Minaire

Postdelivery anal function in primiparous females: Ultrasound and manometric study

PURPOSE: A study was performed to evaluate the early morphologic and functional consequences of vaginal delivery on the anal sphincter in primiparous females. METHODS: Among a cohort of 197 primiparous females who agreed to participate in a clinical evaluation of fecal incontinence and in a transanal ultrasound examination 12 weeks after delivery, 52 also underwent anal manometry using a radial six-port catheter, of whom 10 were asymptomatic and had a normal sphincter at ultrasound and the remaining 42 had clinical signs of anal incontinence or ultrasonographic defects of the anal sphincter or both. Anal sphincter pressures and asymmetry index were analyzed at rest and during voluntary squeeze. Manometric and ultrasound results were compared, together with clinical symptoms. RESULTS: Fourteen patients with clinical signs of anal incontinence had lower resting and squeeze anal pressures than continent patients (P<0.05), but similar anal asymmetry indexes. Patients with incontinence and an anal defect had the lowest resting and squeeze anal pressures (P<0.05). Forceps assistance to delivery was not associated with a higher frequency of anal sphincter lesions. Resting and squeeze anal pressures were lower in the forceps group (P<0.005), but anal asymmetry indexes were similar. Finally, manometric results were identical in the presence or absence of anal sphincter endosonographic defects. CONCLUSIONS: Anal sphincter defects are frequent after the first vaginal delivery, but are not always associated with functional or clinical abnormalities. Resting and squeeze anal pressures were significantly decreased in patients with incontinence and an anal defect and after forceps-assisted deliveries. Anal asymmetry index was not found useful in this population of young primiparous females.

Human hepatic macrovesicular steatosis : a noninvasive study of mitochondrial ketoisocaproic acid decarboxylation

Differentiating between alcoholic and nonalcoholic hepatic steatosis is often a difficult clinical task. However, decreased fatty acid mitochondrial oxidation appears as the main factor for alcoholic steatosis, whereas nonalcoholic steatosis may be due to other causes. We studied mitochondrial function, based on a 13C-ketoisocaproic acid (13C-KIC) breath test, in nine alcoholic and 12 nonalcoholic steatosis patients and 10 healthy volunteers. Our results showed a 42% 13C-KIC decarboxylation decrease in alcoholic steatosis patients, but not in nonalcoholic steatosis patients. This noninvasive breath test appears helpful for the diagnostic work-up of hepatic steatosis.

Glucose and glycogen as fuels for thermogenesis in cold exposed dogs

Abstract The effect of cold-exposure on carbohydrate metabolism was investigated in normothermic dogs using continuous ( 14 C) glucose infusion. Experiments were performed at various ambient temperatures. O 2 consumption ranged from 5.5 to 40 ml O 2 /kg. min. Cold-exposure induced: 1. 1) a non linear rise in plasma glucose turnover and oxidation rates, 2. 2) an increased oxidation/turnover ratio from 0.43 to 0.65, 3. 3) a drop in glucose participation in CO 2 output from 19 to 12 %, 4. 4) a shifting of the carbohydrate metabolism towards muscular glycogen utilization. During the 3 hours cold-exposure period, the hepatic glucose output was about 2.75 g/100 of liver. This result provides further support for hypothesis that the availability of glucose can be a limiting factor at such a high energy expenditure level.

Free fatty acids as the major fuel for thermogenesis in dogs

Abstract The effect of cold-exposure on plasma FFA was investigated in normothermic dogs using continuous infusion of [ 14 C] palmitic acid. The experiments were performed at a neutral ambient temperature (O 2 consumption below 10 ml/kg. min) and at - 25° C (O 2 consumption from 25 to 40 ml/kg. min). The cold-exposure induced: 1. 1) an increase in plasma FFA which was 1.88 times higher than in resting dogs, 2. 2) a rise in turnover and oxidation rates which were respectively 4.5 and 8.3 times above resting values, 3. 3) an increased oxidation/turnover ratio from 0.38 to 0.71, 4. 4) a rise in FFA participation in CO 2 output from 36 to 64 %. In conclusion, the largest part of the energy supply in acute cold-exposed dogs is provided by adipose tissue.

Effect of growth hormone deficiency on hormonal control of hepatic glycogenolysis in hypophysectomized rat

The present study was designed to investigate the hormonal regulation of rat liver glycogenolysis in growth hormone (GH) deficiency. To this end, hepatocytes were isolated from control, GH-deprived (hypophysectomized and treated with triiodothyronine [T3] and corticotropin), and 7-day GH-supplemented fed rats and incubated with glucagon and alpha 1-adrenergic agonist (phenylephrine) to measure the hormonal activation of both glycogen phosphorylase and glucose production from glycogen stores. GH deficiency induces a combined decrease of 50% of the glycogen content, the activity of glucose-6-phosphatase, and the maximal hormone-induced glycogen phosphorylase activity. Daily GH injections restore the levels of both glycogen phosphorylase and glucose-6-phosphatase. These enzymatic inductions occur without normalization of insulinemia. Despite the reduced levels of key enzymes of glycogenolysis, the stimulation of glucose production from glycogen in response to glucagon and phenylephrine is not modified in GH-deprived rats. An increase in the intrinsic activity of one or both of the enzymatic steps is postulated to compensate for the lower levels of enzymes, as indicated by the slopes of the correlation between glucose production and phosphorylase a activity (107 and 216 nmol glucose produced/min/U phosphorylase a [P < .001] in control and GH-deprived rats, respectively). GH replacement enhances maximal phosphorylase activity and brings the correlation toward the control value (slope, 128 nmol glucose produced/min/U phosphorylase a). Our findings demonstrate that glycogenolysis in hepatocytes isolated from GH-deprived rats is normal, despite a reduction of glycogen phosphorylase and glucose-6-phosphatase activities.(ABSTRACT TRUNCATED AT 250 WORDS)