Objective: To assess whether b-glucan (which is fermented in the colon) lowers postprandial glucose concentrations through mechanisms distinct from a delayed carbohydrate absorption and inhibits de novo lipogenesis. Design: Administration of frequent small meals each hour over 9 h allows a rate of intestinal absorption to be reached which is independent of a delayed absorption. A group of 10 healthy men received either an isoenergetic diet containing 8.9 gaday b-glucan or without b-glucan for 3 days. On the third day, the diet was administered as fractioned meals ingested every hour for 9 h. Setting: Laboratory for human metabolic investigations. Subjects: Ten healthy male volunteers. Main outcome measures: Plasma glucose and insulin concentrations, glucose kinetics, glucose oxidation, de novo lipogenesis. Results: On the third day, plasma glucose and free fatty acid concentrations, carbohydrate and lipid oxidation, and energy expenditure were identical with b-glucan and cellulose. Plasma insulin concentrations were, however, 26% lower with b-glucan during the last 2 h of the 9 h meal ingestion. Glucose rate of appearance at steady state was 12% lower with b-glucan. This corresponded to a 21% reduction in the systemic appearance rate of exogenous carbohydrate with b-glucan, while endogenous glucose production was similar with both diets. De novo lipogenesis was similar with and without b-glucan. Conclusion: Administration of frequent meals with or without b-glucan results in similar carbohydrate and lipid metabolism. This suggests that the lowered postprandial glucose concentrations which are observed after ingestion of a single meal containing b-glucan are essentially due to a delayed and somewhat reduced carbohydrate absorption from the gut and do not result from the effects of fermentation products in the colon. Descriptors: glucose production; de novo lipogenesis; substrate oxidation

Our results suggest that an adapted diet containing specific long-chain polyunsaturated fatty acids, prebiotics and probiotics can revert the negative imprinting of neonatal stress on both intestinal barrier function and growth.

ABSTRACT. An abnormality in galactosylation of complex carbohydrates may be important in the pathogenesis of the long-term complications of classic (galactose-lphosphate uridyltransferase-deficient) galactosemia. The ability of nine galactosemic fibroblast preparations to be galactosylated with a purified galactosyltransferase was measured as an indicator of vacant sites where galactose would normally reside. The amount of galactose transferred to cell protein from galactosemic patients was significantly higher than that transferred to a group of seven controls (p < 0.005). Galactosyltransferase activity of the galactosemic cell preparation toward N-acetylglucosamine was also significantly higher than normal (p < 0.01), and there was a linear relationship between these two parameters in galactosemic but not normal cells. These findings suggest that there is defective galactosylation of galactosemic cell complex carbohydrates and that such cells increase their galactosyltransferase levels in an attempt to compensate for the defect. Defective galactosylation may be implicated as an etiologic factor in complications observed in galactosemic patients even when treated with galactose-restricted diets. (Pediatr Res 31: 508-511, 1992) Abbreviations UDPgalactose, uridine diphosphogalactose UDPglucose, uridine diphosphoglucose OPCA, olivopontocerebellar atrophy Although dietary restriction of galactose has been the basis for treatment of classical galactosemia for over 50 years (I), the longterm efficacy of this approach has been seriously questioned. A survey of over 300 patients indicates that even well-treated patients whose galactose restriction was initiated at birth have developmental delay, speech abnormalities, and ovarian failure in females (2). Older galactose-restricted patients have developed an ataxia syndrome (3).Two theories have been proposed, both involving the sugar nucleotide UDPgalactose, to explain the presence of the complications seen despite the absence of dietary galactose. Gitzelmann et al. (4) (7) recently found that the galactose to mannose ratio is abnormally low in a hydrolysate of the cultured fibroblasts of galactosemic patients, supporting the idea of defective galactosylation in these cells. To test the latter hypothesis, we studied the galactosylation state of glycoproteins in cultured fibroblasts by determining the extent to which cellular glycoproteins would serve as galactose acceptors when extracts were incubated with a purified galactosyltransferase. The rationale for this approach was that an impairment of galactosylation would result in a greater number of glycoprotein oligosaccharides being terminated in N-acetylglucosamine. Normally, galactose is linked to N-acetylglucosamine in the biosynthesis of the carbohydrate moieties of glycoproteins by a galactosyltransferase (Fig. 1). We reasoned that if we incubated cell extracts with radiolabeled UDPgalactose and purified galactosyltransferase, radioactive galactose would be transferred to terminal N-acetylglucosamine sites (Fig. 1)....

No abstract

The dopamine (DA) content of the locus coeruleus (LC) and the uptake of tritiated DA in the presence of desmethylimipramine into fresh vibratome sections of the LC-area were determined in control rats and in rats whose ventral tegmental area (VTA) had been destroyed by local application of 6-hydroxydopamine (6-OHDA). Destruction of the VTA reduced the DA content and the number of dopaminergic fibers visualized by radioautography in the LC area. This indicates that the DA containing afferents of the LC originate, at least partly, in the VTA.

Specific carbohydrates, i.e. prebiotics such as fructo-oligosaccharide (FOS), are not digested in the small intestine but fermented in the colon. Besides beneficial health effects of an enhanced bifidobacteria population, intestinal gas production resulting from fermentation can induce abdominal symptoms. Partial replacement with slowly fermented acacia gum may attenuate side effects. The aim was to compare the effects of FOS with those of a prebiotic mixture (50 % FOS and 50 % acacia gum; BLEND) and a rapidly absorbed carbohydrate (maltodextrin) on general intestinal wellbeing, abdominal comfort and anorectal sensory function. Twenty volunteers (eight male and twelve female; age 20-37 years) completed this double-blind, randomised study with two cycles of a 2-week run-in phase (10 g maltodextrin) followed by 5 weeks of 10 g FOS or BLEND once daily, separated by a 4-week wash-out interval. Abdominal symptoms and general wellbeing were documented by telephone interview or Internet twice weekly. Rectal sensations were assessed by a visual analogue scale during a rectal barostat test after FOS and BLEND treatment. Both FOS and BLEND induced more side effects than maltodextrin. Belching was more pronounced under FOS compared with BLEND (P¼ 0·09 for females; P¼0·01 for males), and for self-reported general wellbeing strong sex differences were reported (P¼0·002). Urgency scores during rectal barostat were higher with FOS than BLEND (P¼ 0·01). Faced with a growing range of supplemented food products, consumers may benefit from prebiotic mixtures which cause fewer abdominal side effects. Sex differences must be taken in consideration when food supplements are used.

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Pinch-induced catalepsy was readily obtained in five strains of mice following repeated administration of strong pinches at the scruff of the neck. This catalepsy outlasted the pinch by minutes and was more easily induced on retests 48 hr after the initial acquisition test. Repetitive tail pinches and/or exposure to the testing procedure without pinches also resulted in immobility; however, this was weak in magnitude and short in duration. Treatments designed to prevent immobility between trials (swimming in water or housing in the home cage with normally behaving littermates) failed to block or modify pinch-induced catalepsy. Spacing the trials up to one pinch per 10 min did not affect the emergence of pinch-induced catalepsy, but at one pinch per 30 min it was abolished. Pinch-induced catalepsy is strikingly similar to the behavior elicited in mice when attacked by a cat. In both cases, immobility is produced by pinches or bites at the scruff of the neck, and it outlasts the duration of the stimulus. These results support the notion of pinch-induced catalepsy as an adaptive coping strategy, increasing the chance of survival in predator/prey confrontations.