To explore mechanisms underlying triglyceride (TG) accumulation in livers of chow-fed apo E-deficient mice (Kuipers, F., J.M. van Ree, M.H. Hofker, H. Wolters, G. In't Veld, R.J. Vonk, H.M.G. Princen, and L.M. Havekes. 1996. Hepatology. 24:241-247), we investigated the effects of apo E deficiency on secretion of VLDL-associated TG (a) in vivo in mice, (b) in isolated perfused mouse livers, and (c) in cultured mouse hepatocytes. (a) Hepatic VLDL-TG production rate in vivo, determined after Triton WR1339 injection, was reduced by 46% in apo E-deficient mice compared with controls. To eliminate the possibility that impaired VLDL secretion is caused by aspecific changes in hepatic function due to hypercholesterolemia, VLDL-TG production rates were also measured in apo E-deficient mice after transplantation of wild-type mouse bone marrow. Bone marrow- transplanted apo E-deficient mice, which do not express apo E in hepatocytes, showed normalized plasma cholesterol levels, but VLDL-TG production was reduced by 59%. (b) VLDL-TG production by isolated perfused livers from apo E-deficient mice was 50% lower than production by livers from control mice. Lipid composition of nascent VLDL particles isolated from the perfusate was similar for both groups. (c) Mass VLDL-TG secretion by cultured apo E-deficient hepatocytes was reduced by 23% compared with control values in serum-free medium, and by 61% in the presence of oleate in medium (0. 75 mM) to stimulate lipogenesis. Electron microscopic evaluation revealed a smaller average size for VLDL particles produced by apo E-deficient cells compared with control cells in the presence of oleate (38 and 49 nm, respectively). In short-term labeling studies, apo E-deficient and control cells showed a similar time-dependent accumulation of [3H]TG formed from [3H]glycerol, yet secretion of newly synthesized VLDL-associated [3H]TG by apo E-deficient cells was reduced by 60 and 73% in the absence and presence of oleate, respectively. We conclude that apo E, in addition to its role in lipoprotein clearance, has a physiological function in the VLDL assembly-secretion cascade.

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SUMMARY Intestinal D-fructose absorption in 31 children was investigated using measurements of breath hydrogen. Twenty five children had no abdominal symptoms and six had functional bowel disorders. After ingestion of fructose (2 g/kg bodyweight), 22 Fructose is used with increasing frequency in a number of foods, especially beverages. Since its incomplete absorption may lead to recurrent abdominal pain, we decided to investigate fructose absorption in children, measuring the hydrogen concentration in expired air after a fructose challenge. Subjects and methodsWe studied 31 children aged between 1 month and 16 years 9 months (mean 7-7 years). Twenty five children were completely free of gastrointestinal symptoms but six had functional abdominal complaints. None of the children had received antibiotics or cytotoxic treatment in the days before the tests. The parents gave informed consent and some were present during the test.Fructose was given as a 20% solution at a dose of 2 g/kg body weight (maximum 50 g) after a fast of at least six hours. Duplicate breath samples were taken immediately before administration of the fructose solution and at 30 minute intervals thereafter for two and a half hours, using a modification of the method of Douwes et al.6 The samples were stored in vacuum tubes. The hydrogen concentration of the samples was assessed using a Hewlett Packard HP 5880 gas chromatograph and a thermal conductivity detector. A 50 cm stainless steel column filled with molecular sieve 5A was flushed with nitrogen, 12 ml per minute. The oven temperature was 60°C and the detector temperature 300°C. Any abdominal symptoms present during the test were noted. The results were corrected for the basal breath hydrogen value which ranged from 4 to 23 ppm in 30 children and was 114 ppm in one. The peak increase in breath hydrogen was determined: a peak increase of more than 10 ppm was considered indicative of incomplete absorption of fructose.7 Seven children were 735 on 27 April 2019 by guest. Protected by copyright.

Background Schizophrenia is associated with lower intelligence and poor educational performance relative to the general population. This is, to a lesser degree, also found in first-degree relatives of schizophrenia patients. It is unclear whether bipolar disorder I (BD-I) patients and their relatives have similar lower intellectual and educational performance as that observed in schizophrenia. Methods This cross-sectional study investigated intelligence and educational performance in two outpatient samples (494 BD-I patients, 952 schizophrenia spectrum (SCZ) patients), 2,231 BD-I and SCZ relatives patients, 1,104 healthy controls and 100 control siblings. Mixed-effects- and regression models were used to compare groups on intelligence and educational performance. Results BD-I patients were more likely to have completed the highest level of education (OR=1.88 [1.66–2.70]) despite having a lower IQ compared with controls (β=−9.09, SE=1.27, p<0.001). In contrast, SCZ patients showed both a lower IQ (β= −15.31, SE=0.86, p<0.001) and lower educational levels compared with controls. Siblings of both patient groups had significantly lower IQ than control siblings, but did not differ on educational performance. IQ scores did not differ between BD-I parents and SCZ parents, but BD-I parents had completed higher educational levels. Conclusions Although BD-I patients had a lower IQ than controls, they were more likely to have completed the highest level of education. This contrasts with SCZ patients, who showed both intellectual and educational deficits compared to healthy controls. Since relatives of BD-I patients did not demonstrate superior educational performance, our data suggest that high educational performance may be a distinctive feature of bipolar disorder patients.

Lactose maldigestion and intolerance affect a large part of the world population. The underlying factors of lactose intolerance are not fully understood. In this review, the role of colonic metabolism is discussed, i.e. fermentation of lactose by the colonic microbiota, colonic processing of the fermentation metabolites and how these processes would play a role in the pathophysiology of lactose intolerance. We suggest that the balance between the removal and production rate of osmotic-active components (lactose, and intermediate metabolites, e.g. lactate, succinate, etc.) in the colon is a key factor in the development of symptoms. The involvement of the colon may provide the basis for designing new targeted strategies for dietary and clinical management of lactose intolerance.