Changes in lipid profile variables in response to submaximal and maximal exercise in trained cyclists

This study examined the effect of prolonged submaximal exercise followed by a self-paced maximal performance test on cholesterol (T-Chol), triglycerides (TG), and high-density lipoprotein cholesterol (HDLC). Nine trained male athletes cycled at 70% of maximal oxygen consumption for 60 min, followed by a selfpaced maximal ride for 10 min. Venous blood samples were obtained at rest, at 30 and 60 min during submaximal exercise, and immediately after the performance test. Lactic acid, haematocrit (Hct), haemoglobin (Hb), T-Chol and TG were measured in the blood, while plasma was assayed for HDL-C. Plasma volume changes in response to exercise were calculated from Hct and Hb values and all lipid measurements were corrected accordingly. In order to ascertain the repeatability of lipid responses to exercise, all subjects were re-tested under identical testing conditions and experimental protocols. When data obtained during the two exercise trials were analysed by two-way ANOVA no significant differences (P > 0.05) between tests were observed. Consequently the data obtained during the two testing trials were pooled and analysed by one-way ANOVA. Blood lactic acid increased non-significantly (P > 0.05) during the prolonged submaximal test, but rose markedly (P < 0.05) following the performance ride. Lipid variables ascertained at rest were within the normal range for healthy subjects. ANOVA showed that blood T-Chol and TG were unchanged (P > 0.05), whereas HDL-C rose significantly (P < 0.05) in response to exercise. Post hoc analyses indicated that the latter change was due to a significant rise in HDL-C after the performance ride. It is concluded that apparent favourable changes in lipid profile variables occur in response to prolonged submaximal exercise followed by maximal effort, and these changes showed a good level of agreement over the two testing occasions.     

Familial Similarities of Changes in Cognitive, Behavioral, and Physiological Variables in a Cardiovascular Health Promotion Program

A number of studies have demonstrated that physiological andbehavioral cardiovascular disease (CVD) risk factors aggregatewithin families. This fact, and the potential mediating rolethat the family plays in behavior change, have led to the developmentof family-based CVD risk reduction programs, including the SanDiego Family Health Project. The aggregation of behavioral,physiological, and cognitive changes within families was assessedduring a 1-year intervention. We found evidence of modest butsignificant aggregation of change. There was more aggregationof change in behavioral variables than in physiological or cognitivevariables. More significant correlations were found among 3-dayfood record measures than among 24-hour recall dietary measures,suggesting an influence of assessment method. Aggregation ofchange within families was stronger within generations thanacross generations. These data point to the importance of involvingall age groups in health promotion programs.     

Effects of apolipoprotein A-IV genotype on glucose and plasma lipoprotein levels

The effects of apolipoprotein (apo) A-IV genotype on serum glucose, total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, triglyceride and glucose concentrations were ascertained in a population of 373 men and 361 women with a mean age of about 57 years. Subjects were evaluated at entry into a lifestyle intervention program. Apolipoprotein A-IV genotype variations at residues 347 and 360 were examined, as these mutations affect the sequence of apo A-IV, a major protein constituent of intestinal triglyceride-rich lipoprotein and HDL. With regard to the apo A-IV 360 mutation, 16.4% of the females and 13.4% of the males carried the apo A-IV 2-allele, almost entirely in the heterozygous state. No effect of the apo A-IV 1/2 genotype was observed in either men or women on total cholesterol, LDL cholesterol, HDL cholesterol, triglyceride, the total cholesterol (TC)/HDL ratio, or on A-I, A-IV and apo B levels. This was also the case for the apo A-IV 347 mutation. However, women with the apo A-IV 360 1/2 genotype had significantly (p < 0.005) higher glucose levels (105.5 mg/dl) compared with the 1/1 wild-type (94.0 mg/dl). All analyses were also adjusted for age, body mass index, medications, alcohol use and cigarette smoking. The prevalence of the 347 mutation was somewhat higher than the 360 mutation, with 29% of the females and 32.0% of the males being heterozygous for this mutation, and 3.9% of the females and 5.4% of the males being homozygous for this mutation. These data are consistent with the concept that the apo A-IV 360 and 347 genotypes have no significant effect on apo A-IV levels and other lipid parameters in either gender. However, apo A-IV 360 1/2 genotype did have a significant effect on serum glucose levels in women.     

Apolipoprotein B gene DNA polymorphisms are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus

Ukkola O, Savolainen MJ, Salmela PI, von Dickhoff K, Kesäniemi YA. Apolipoprotein B gene DNA polymorphisms are associated with macro-and microangiopathy in non-insulin-dependent diabetes mellitus. Clin Genet 1993: 44: 177–184. © Munksgaard, 1993 The relationship between diabetic macroangiopathy or microangiopathy and apolipoprotein B (apoB) polymorphism was studied in 139 male and 129 female patients with non-insulin-dependent diabetes (NIDDM) mellitus, comprising consecutive patients with poor diabetic control (HBA1 13.2%\pm2.7 (SD)) referred to our hospital. Plasma cholesterol and triglyceride concentrations were higher in the patients who were homozygous for the X2 allele (presence of Xba I cleavage site). Patients with the X1 allele (absence of Xba I cleavage site) tended to have a higher frequency of macroangiopathy, although the differences were not statistically significant. There was no difference in the prevalence of microangiopathy between the groups. In subjects with only an R1 allele (= R +; homozygous for the presence of EcoR I cleavage site) the prevalence of coronary heart disease (CHD) was observed to be high (61.9%) as compared to the subjects possessing an R2 allele (= R —; homozygous or heterozygous for the absence of the EcoR I cleavage site) (46.7%; p<0.02). When the polymorphisms Xba I (subjects homozygous for the absence of the cutting site = X +; subjects homozygous or heterozygous for the presence of the cutting site = X —) and EcoR I were combined, the prevalence of macroangiopathy was observed to be high in X + R + (80.0%) as compared with X + R- (44.2%), X-R+ (56.8%) and X-R- (50.0%) (p<0.03). The prevalence of macroangiopathy tended to be particularly high in patients with the apoprotein E4 allele (phenotype E4\4 or E4/3), combined with either X+ or R +. Our findings suggest that variation at the apoB locus is one of the factors involved in predisposing diabetic patients to the development of arterial disease. As in previous studies the effect of the variation at the apoB gene on circulating lipid levels was observed. The data also support a role for the e4 allele of the apolipoprotein E gene as an important determinant of macroangiopathy in NIDDM.     

Apolipoprotein B-100 gene Xba I polymorphism and cholesterol gallstone disease

The apolipoprotein (apo) B gene Xba I polymorphism is associated with alterations in serum lipids. Disturbances in serum lipids may be a risk factor for cholesterol gallstone disease. However, the relation between the Xba I polymorphism and cholesterol gallstones is unknown. This study was aimed at characterizing the polymorphism of the apo B gene Xba I in patients with gallbladder stones and the association of Xba I polymorphism with serum lipids. Xba I genotypes were measured by PCR-RFLP, and serum lipids assayed in 190 patients with gallbladder stones and 441 control subjects. The frequency of the X+/- genotype (20.63 vs. 7.94%) and X+ allele (10.79 vs. 3.97%) was significantly higher in the patient group than in the control group. Patients with the X+/- genotype had a significantly higher concentration of total cholesterol, low-density lipoprotein (LDL)-cholesterol, and apo B in serum than patients with the X-/- genotype. The X+ allele of the apo B gene is characterized by a higher cholesterol concentration and a higher LDL-cholesterol concentration in serum, and it may be a marker for increased risk of cholesterol gallstone disease.     

Cell cholesterol esters and high-density lipoprotein plasma levels during liver hyperplasia in choline-fed male and female rats

Sexual dimorphism exists in the response of rats to lead nitrate, liver hyperplasia occuring earlier and being more pronounced in males. Excess dietary choline in females shifted the growth pattern towards that of males. To determine whether phosphatidylcholine-induced growth modulations could be related to a derangement of cholesterol metabolism, liver accumulation of cholesterol esters and plasma lipoprotein patterns were investigated. In males, lead-induced liver hyperplasia was associated with increased total cholesterol hepatic content, accumulated cholesterol esters and reduced concentration of plasma High Density Lipoprotein (HDL) cholesterol. Females were less responsive to the liver mitogenic signal of lead nitrate; there was no elevation of cholesterol content nor any marked accumulation of cholesterol esters. This is consistent with the lack of change in the plasma levels of HDL cholesterol. Continuous choline feeding displaced the liver cholesterol ester pattern and plasma HDL cholesterol levels in females, and in parallel that of DNA synthesis, towards those of males. Choline was not observed to have any effect in males. These results suggest that the derangement of phosphatidylcholine metabolism induces growth-related changes in cholesterol turnover; they are consistent with the proposal that the intracellular content of cholesterol esters may have a role in regulating liver growth rates.     

Behavior of 3-year-old children in a prospective randomized trial of reduced saturated fat and cholesterol diet since infancy: The strip baby project

Interventions aimed at decreased exposure of children to known atherosclerosis risk factors may have untoward behavioral side effects. We examined how children’s behavior or parent’s perception of the behavior of the children at 3 years of age was influenced by the intervention in a prospective randomized trial that began in infancy and effectively decreased scrum cholesterol concentration. This Special Turku coronary Risk factor Intervention Project for babies (STRIP) began when the infant was 7 months old. Half of 1.062 children received individualized dietary counseling at 1-to 3-month intervals during the first 2 years of age and then half-yearly; the other half had an unrestricted diet. At 3 years of age a standardized questionnaire of the child’s behavior was sent to 791 families (76% returned the questionnaire). At the onset of the trial the sociodemographic data of the families and scrum lipid values of the intervention and control children were similar. Later, mean serum cholesterol values of the intervention children remained constantly at a level 6% to 10% below the values of the control children. At 3 years of age the parental perceptions of the child’s behavior suggested minimal differences between the intervention and control children. The intervention children were slightly less jealous and more active and creative, but showed slightly more negative signs of behavior (bed-wetting, problems in falling asleep, fears) than the controls. We conclude that long-term, individualized dietary and lifestyle intervention that begins in infancy slightly influences children’s behavior or parent’s recognition of the behavior of the children at the age of 3 years. This work was supported in part by grants from the Varsinais-Suomi Regional Fund of the Finnish Cultural Foundation, the Mannerheim League for Child Welfare, the Academy of Finland, and the Alli Paasikivi Foundation.     

Holoprosencephaly: from Homer to Hedgehog

Holoprosencephaly (HPE), a common developmental defect affecting the forebrain and face, is etiologically heterogeneous and exhibits wide phenotypic variation. Graded degrees of severity of the brain malformation are also reflected in the highly variable craniofacial malformations associated with HPE. In addition, individuals with microforms of HPE, who usually have normal cognition and normal brain imaging, are at risk for having children with HPE. Some obligate carriers for HPE may not have any phenotypic abnormalities. Recurrent chromosomal rearrangements in individuals with HPE suggest loci containing genes important for brain development, and abnormalities in these genes may result in HPE. Recently, Sonic Hedgehog (SHH) was the first gene identified as causing HPE in humans. Proper function of SHH depends on cholesterol modification. Other candidate genes that may be involved in HPE include components of the SHH pathway, elements involved in cholesterol metabolism, and genes expressed in the developing forebrain.