Relation of Serum Cholesterol to in vitro 7α-Dehydroxylation of Primary Bile Acids by Fecal Bacteria in Infants and Children

PEDIATRICS ◽  
1974 ◽  
Vol 54 (2) ◽  
pp. 222-228
Author(s):  
Paul Samuel ◽  
Arnold Schussheim ◽  
Sidney Lieberman ◽  
Eugene C. Don

Fresh feces from 104 infants and children (aged 3 days to 16 years) were homogenized and incubated with labeled cholic or chenodeoxycholic acid. After 2 and/or 24 hours' incubation, the percentage of converted (mostly 7α-dehydroxylated) primary bile acids was measured, and the degree of conversion was correlated with serum cholesterol levels. It was found that stool homogenates of patients with low levels of serum cholesterol (< 160 mg/100 ml) converted labeled primary bile acids poorly or not at all, whereas in patients with higher serum cholesterol levels (> l60 mg/100 ml) the conversion process was markedly increased. Thus, highly significant correlations were found between serum cholesterol levels and the capability of the fecal bacterial flora to convert both primary bile acids "in vitro." The possibility is proposed that in man the relatively rapid progressive increase of serum cholesterol level following birth may be related to the colonization of the intestinal tract by 7α-dehydroxylating and/or bile acid degrading bacteria. It is suggested that the prevalence of these bacteria is subject to environmental effects, and it may be one of the important factors regulating cholesterol levels in man.

1980 ◽  
Vol 43 (1) ◽  
pp. 95-100 ◽  
Author(s):  
S. A. Jenkins

1. Pregnant guinea-pigs receiving a low dose of L-ascorbic acid (0.2 mg/100 g body-weight per d) developed a hypercholesterolaemia in the third trimester of pregnancy, whereas no change in serum cholesterol levels was observed in pregnant animals receiving a higher dose of the vitamin (2 mg/100 g body-weight per d).2. Pregnancy in the group of guinea-pigs receiving the higher dose of L-ascorbic acid was associated with an increased biliary secretion of bile acids. No change was observed in the biliary secretion of bile acids in pregnant animals receiving the lower dose of L-ascorbic acid, but these animals secreted significantly more cholesterol.3. Changes in the biliary secretion of cholesterol and bile acids in the pregnant guinea-pig according to L-ascorbic acid intake were reflected in the composition of the gall-bladder bile. Thus, the gall-bladder bile of guinea-pigs receiving the lower dose of L-ascorbic acid contained more cholesterol, while the gall-bladder bile of those animals receiving the higher dose of the vitamin had a higher content of bile acids.4. The increased cholesterol content of the gall-bladder of pregnant guinea-pigs receiving the lower dose of L-ascorbic acid resulted in decreased bile acid:cholesterol and phospholipid: cholesterol values, conditions predisposing to cholelithiasis.


2012 ◽  
Vol 36 (0E) ◽  
pp. 190-193
Author(s):  
Jameel G. H.

Sixty cows were included in this study which was conducted in Baquba for the period from April 2011 to October 2011. They were clinically diagnosed as having bovine ephemeral fever (BEF) infection. Blood samples were collected from infected cows before, after treatment, and after recovery. Additionally, 30 healthy cows were included as control group. Sera were separated and submitted for the determination of phosphorus, glucose, cholesterol and pH levels. Statistical analysis of biochemical values revealed significant decrease in serum cholesterol levels in infected cows as compared to control group (P<0.05). Furthermore, the diseased cows showed low levels of pH (acidosis), thus when they treated by intravenous injection of 5% sodium bicarbonate, the signs were rapidly subsided and the cows were completely recovered.


2017 ◽  
Vol 95 (1) ◽  
pp. 142-147 ◽  
Author(s):  
Kanae Nakamura ◽  
Satoru Morishita ◽  
Tomoji Ono ◽  
Michiaki Murakoshi ◽  
Keikichi Sugiyama ◽  
...  

Lactoferrin (LF) is a multifunctional cationic protein (pI 8.2–8.9) in mammalian milk. We previously reported that enteric-LF prevented hypercholesterolemia and atherosclerosis in a diet-induced atherosclerosis model using Microminipig, although the underlying mechanisms remain unclear. Because LF is assumed to electrostatically interact with bile acids to inhibit intestinal cholesterol absorption, LF could promote cholesterol excretion. In this study, we assessed the interaction between LF and taurocholate in vitro, and the effect of LF on cholesterol excretion in rats. The binding rate of taurocholate to LF was significantly higher than that to transferrin (pI 5.2–6.3). When rats were administered a high-cholesterol diet (HCD) containing 5% LF, LF was detected using ELISA in the upper small intestine from 7.5 to 60 min after the administration. Rats were fed one of the following diets: control, HCD, or HCD + 5% LF for 21 days. Fecal neutral steroids and hepatic cholesterol levels in the HCD group were significantly higher than those in the control group. The addition of LF to a HCD significantly increased fecal neutral steroids levels (22% increase, p < 0.05) and reduced hepatic cholesterol levels (17% decrease, p < 0.05). These parameters were inversely correlated (R = −0.63, p < 0.05). These results suggest that LF promotes cholesterol excretion via interactions with bile acids.


2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Marion Koch ◽  
Jaimini Cegla ◽  
Ben Jones ◽  
Yuning Lu ◽  
Ziad Mallat ◽  
...  

Abstract Background Malaria disease commences when blood-stage parasites, called merozoites, invade human erythrocytes. Whilst the process of invasion is traditionally seen as being entirely merozoite-driven, emerging data suggests erythrocyte biophysical properties markedly influence invasion. Cholesterol is a major determinant of cell membrane biophysical properties demanding its interrogation as a potential mediator of resistance to merozoite invasion of the erythrocyte. Methods Biophysical measurements of erythrocyte deformability by flicker spectroscopy were used to assess changes in erythrocyte bending modulus on forced integration of cholesterol and how these artificial changes affect invasion by human Plasmodium falciparum merozoites. To validate these observations in a natural context, either murine Plasmodium berghei or human Plasmodium falciparum merozoites were tested for their ability to invade erythrocytes from a hypercholesterolaemic mouse model or human clinical erythrocyte samples deriving from patients with a range of serum cholesterol concentrations, respectively. Results Erythrocyte bending modulus (a measure of deformability) was shown to be markedly affected by artificial modulation of cholesterol content and negatively correlated with merozoite invasion efficiency. In an in vitro infection context, however, erythrocytes taken from hypercholesterolaemic mice or from human clinical samples with varying serum cholesterol levels showed little difference in their susceptibility to merozoite invasion. Explaining this, membrane cholesterol levels in both mouse and human hypercholesterolaemia erythrocytes were subsequently found to be no different from matched normal serum controls. Conclusions Based on these observations, serum cholesterol does not appear to impact on erythrocyte susceptibility to merozoite entry. Indeed, no relationship between serum cholesterol and cholesterol content of the erythrocyte is apparent. This work, nonetheless, suggests that native polymorphisms which do affect membrane lipid composition would be expected to affect parasite entry. This supports investigation of erythrocyte biophysical properties in endemic settings, which may yet identify naturally protective lipid-related polymorphisms.


2019 ◽  
Vol 78 (9) ◽  
pp. 798-807
Author(s):  
Kampei Shimizu ◽  
Haruka Miyata ◽  
Yu Abekura ◽  
Mieko Oka ◽  
Mika Kushamae ◽  
...  

Abstract Subarachnoid hemorrhage due to rupture of intracranial aneurysms is a life-threatening disease. Although some previous reports have demonstrated an association between lipid accumulation and degenerative changes in aneurysmal walls in humans, epidemiological studies have failed to identify dyslipidemia as a risk factor for intracranial aneurysms. Thus, we examined whether an increase in serum cholesterol levels facilitates the progression of intracranial aneurysms in a rat model. Rats were given a high-fat diet (HFD) and subjected to an intracranial aneurysm model. The HFD elevated their serum cholesterol levels. The intracranial aneurysms induced at the anterior cerebral artery-olfactory artery bifurcation were significantly larger in the high-fat group than in the normal-chow group. Histological analysis demonstrated that the loss of medial smooth muscle layers was exacerbated in the high-fat group and indicated the presence of macrophage-derived foam cells in the lesions. In in vitro experiments, the expression levels of the pro-inflammatory genes induced by LPS in RAW264.7-derived foam cells were significantly higher than those in RAW264.7 cells. The combination of these results suggests that increased serum cholesterol levels facilitate degenerative changes in the media and the progression of intracranial aneurysms presumably through foam cell transformation.


PEDIATRICS ◽  
1976 ◽  
Vol 58 (2) ◽  
pp. 274-282
Author(s):  
Peter J. Savage ◽  
Richard F. Hamman ◽  
Gregory Bartha ◽  
Stephen E. Dippe ◽  
Max Miller ◽  
...  

Serum cholesterol levels from birth to adulthood in a population of North American (Pima) Indians are described and compared to those of Caucasian populations. Cholesterol levels at birth (mean ± SEM, 87 ± 2.6 mg/100 ml) were similar in Pimas and Caucasians, but levels in Pimas from 5 to 16 years (148 ± 4.6 mg/100 ml) were 20 to 30 mg/100 ml lower than among most white populations. The levels showed little rise with age from 5 to 16, then rose significantly in both sexes from ages 17 to 25. Cholesterol levels in adult Pimas (190 ± 1.5 mg/100 ml) were up to 50 to 60 mg/100 ml lower than in American whites, and showed little increase after age 25. Two cohorts of children followed prospectively for six years indicated that the prevalence data reflect sequential changes in the population. Cholesterol levels of those subjects were significantly correlated at the first and last examinations. The Pima, in contrast to Caucasian American populations, have relatively low levels of serum cholesterol and low rates of coronary heart disease, but evidence of a causal relationship with the latter remains to be established.


2020 ◽  
Vol 11 ◽  
Author(s):  
Chen Xing ◽  
Xin Huang ◽  
Yifan Zhang ◽  
Chongchong Zhang ◽  
Wei Wang ◽  
...  

Disturbed sleep is closely associated with an increased risk of metabolic diseases. However, the underlying mechanisms of circadian clock genes linking sleep and lipid profile abnormalities have not been fully elucidated. This study aimed to explore the important role of the circadian clock in regulating impaired cholesterol metabolism at an early stage of sleep deprivation (SD). Sleep disturbance was conducted using an SD instrument. Our results showed that SD increased the serum cholesterol levels. Concentrations of serum leptin and resistin were much lower after SD, but other metabolic hormone concentrations (adiponectin, glucagon, insulin, thyroxine, norepinephrine, and epinephrine) were unchanged before and after SD. Warning signs of cardiovascular diseases [decreased high density lipoprotein (HDL)-cholesterol and increased corticosterone and 8-hydroxyguanosine levels] and hepatic cholestasis (elevated total bile acids and bilirubin levels) were observed after SD. Cholesterol accumulation was also observed in the liver after SD. The expression levels of HMGCR, the critical enzyme for cholesterol synthesis, remained unchanged in the liver. However, the expression levels of liver CYP7A1, the enzyme responsible for the conversion of cholesterol into bile acids, significantly reduced after SD. Furthermore, expression of NR1D1, a circadian oscillator and transcriptional regulator of CYP7A1, strikingly decreased after SD. Moreover, NR1D1 deficiency decreased liver CYP7A1 levels, and SD could exacerbate the reduction of CYP7A1 expression in NR1D1−/− mouse livers. Additionally, NR1D1 deficiency could further increase serum cholesterol levels under SD. These results suggest that sleep disturbance can induce increased serum cholesterol levels and liver cholesterol accumulation by NR1D1 mediated CYP7A1 inhibition.


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