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Physical activity and high -density lipoprotein cholesterol in sedentary male smokersShaw, BS, Shaw, I 16 December 2007 (has links)
High-density lipoprotein (HDL) with its cardio-
protective effects has provided remarkable
optimism to the ever-increasing incidences of
coronary artery disease. Therefore, the aim of this
randomized, comparative, research trial was to
determine whether endurance exercise training,
weight training and/or a combination of aerobic and
weight training can be utilized in the management
of high-density lipoprotein cholesterol (HDL-C).
Subsequent to the 16-week intervention period,
dependant t-Tests revealed that the non-exercising
and weight training groups demonstrated non-
significant mean 1.3% (p = 0.754) and 11.1% (p =
0.069) increases in fasting serum HDL-C,
respectively. Conversely, there was a significant
increase in HDL-C following the 16 weeks of
endurance training (p = 0.003) and combination
training (p = 0.005) (22.4% and 37.9%,
respectively). Further, Spearman’s rho indicated no
correlations between HDL-C and BMI (r = -0.131),
percentage body fat (r = - 0.141), cholesterol intake
(r = - 0.026) and total fat intake (r = - 0.239). The
absence of changes in these inter-correlations
indicated that changes in these parameters had no
effect on the HDL-C. On the contrary, moderate
correlations were established between HDL-C and
number of cigarettes smoked daily (r = - 0.344) and
intake of saturated fat (r = - 0.317) indicating that
exercise effect on these variables could have
indirectly contributed significantly in altering HDL-
C in the endurance and combination training
groups. As such, endurance and combination
training can be utilized as an effective method in the
management of HDL-C in sedentary male smokers.
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The Role of Macrophage Scavenger Receptor Class B, Type 1 (SR-BI) in the development of Atheroscelerosis in Apolipoprotein E Deficient MiceRisvi, Ali Amjad 11 1900 (has links)
The high density lipoprotein (HDL) receptor Scavenger Receptor, Class B, Type I (SRBI)
is a 509 amino acid integral membrane protein which has been shown to have an
important role in HDL-mediated reverse cholesterol transport. SR-BI has been shown to
mediate selective uptake of cholesterol, and also mediates efflux of cholesterol to HDL as
seen in in vitro cell culture studies. SR-BI is abundant in the liver and steroidogenic
tissues, and is also present in macrophages, which play an important role in the initial
stages of atherosclerotic development. SR-BI has been shown to be protective against
atherosclerosis by way of overexpression and knockout (KO) studies in murine
atherosclerosis models, including low density lipoprotein receptor (LDLR) knockout
mice, apolipoprotein E (ApoE) knockout mice, and human apolipoprotein B (ApoB)
transgenic mice. SR-BI/LDLR double knockout (dKO) mice show a 6-fold increase in
diet-induced atherosclerosis compared to LDLR single KO controls, and SR-BI/ApoE
dKO mice show severe coronary occlusion, myocardial infarction, and premature death
on a normal chow diet. In both, plasma total cholesterol levels are significantly elevated,
and associated with abnormally large HDL particles. The majority ofSR-BI's
atheroprotective effect has been shown to result from plasma cholesterol clearance by
way of selective uptake in the liver. Recently, Covey et al showed that elimination of SRBI
expression in macrophages of LDLR KO mice resulted in increased diet-induced
atherosclerosis. To see if SR-BI in macrophages contributes to the overall
atheroprotective effect of SR-BI in ApoE KO mice, presumably by mediating cellular
cholesterol efflux to HDL, selective deletion ofSR-BI was induced in bone marrow
derived cells of ApoE KO mice using bone marrow transplantation. Female ApoE -/recipient
mice were transplanted with either SR-BI +/+ ApoE -/-or SR-BI -/- ApoE -/bone
marrow from male donor mice, and fed a high fat diet for 12 weeks. This resulted in
significantly increased atherosclerosis in mice transplanted with SR-BI -/- ApoE -/-bone
marrow, with a concomitant decrease in cholesterol associated with HDL-sized
lipoproteins. No significant differences were seen in plasma total cholesterol levels or
levels of cholesterol associated with non-HDL lipoproteins. These data suggest that SRBI
in macrophages contributes to SR-BI's overall protective effect against
atherosclerosis, and also plays a role in the regulation ofHDL cholesterol, in ApoE
deficient mice. / Thesis / Master of Science (MSc)
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The association of LDLR and PCSK9 variants with LDL-c levels in a black South African population in epidemiological transition / Tertia van ZylVan Zyl, Tertia January 2013 (has links)
Background
Elevated concentrations of low-density lipoprotein cholesterol (LDL-c) are a major risk factor for the development of coronary artery disease (CAD) because of their role in the progression of atherosclerosis. The black South African population is known to have had historically low LDL-c and in the past there was almost no CAD in the population. However, as this population moves through the nutrition transition, LDL-c levels are increasing. LDL-c levels are regulated by the LDL receptors, which is the major protein involved with transporting cholesterol across cell membranes in humans. Proprotein convertase subtilisinlike/kexin type 9 (PCSK9) is another protein involved with the regulation of LDL-c through its role in assisting with the degradation of the LDL receptor. Variants in both genes can cause elevated or lowered LDL-c levels. Very little information is available on the frequency or presence of variants in the low-density lipoprotein receptor (LDLR) and PCSK9 gene in the black South African population and on how these variants associate with LDL-c. The main aim of the study was thus to determine novel and existing genetic variants in these two genes and to describe the manner in which they associate with plasma LDL-c levels in a black South African population undergoing an epidemiological transition.
Methods
The 2005 baseline data from the Prospective Urban and Rural (PURE) study population were used in this study. The study population consisted of apparently healthy black volunteers form the North West province of South Africa, aged 35 to 60 years. Thirty individuals were randomly chosen from the 1860 volunteers to determine the presence of known and novel variants in these genes by automated bidirectional sequencing. The promoter region, exons and flanking regions were sequenced and variants were identified utilising CLC DNA Workbench. Deoxyribonucleic acid (DNA) samples for 1500 individuals of the PURE study population were genotyped by means of a Golden Gate Genotyping Assay. Analyses of covariance (ANCOVA) were used to test for associations between the different genotypes in both the LDLR and PCSK9 genes and LDL-c levels. Haplotypes were generated by using the confidence intervals on the software programme, HaploView. A genetic risk score (GRS) was determined by including variants which associated significantly with LDL-c. The GRS, the haplotypes and the variants that associated significantly with LDL-c were used in separate linear regression models with variants which correlated with LDL-c to determine how all these variables contribute to the differences in LDL-c levels.
Results and discussion
Novel and known variants were identified in both the genes and in total 52 variants were genotyped. Rare variants such as rs17249141 and rs28362286 were detected in the study population and are associated with low levels of LDL-c. The variants identified in the LDLR gene were situated largely in regulatory regions such as the promoter, intron and 3‟untranslated regions. Haplotypes in the LDLR gene with the highest frequency associated with lower LDL-c levels, which could contribute to the study population‟s low mean LDL-c level. Haplotypes identified in the PCSK9 gene had a weaker association with LDL-c levels. The minor allele frequencies of many of the variants differed from those of the European population and therefore the importance of population-specific research cannot be sufficiently emphasised. The GRS, haplotypes and variants used in the regression models to determine whether they contributed to predicting the variance in LDL-c in the study population made a small contribution to explaining this. BMI best explained the variance in LDL-c levels. Older women with a body mass index (BMI)>25kg/m2 were identified as being at greater risk of developing elevated LDL-c levels than the rest of the study population. Heterozygote carriers of variant, rs28362286, had 0.787 mmol/L lower LDL-c than carriers of the wild type and this is associated with a reduced risk of developing CAD.
Conclusion and recommendation
When considering the results mentioned above, adding genetic analysis to explaining the variance in LDL-c levels seems to have its limitations, but the study included only two of many genes that play a role in the metabolism and regulation of LDL-c levels. Incorporating more genes and more variants into analyses and prediction models will add greater value to defining LDL-c levels. Rarer variants with a large impact on protein function, such as rs28362286, have a greater effect on LDL-c levels and could predict the variance better than the common variants. Risk factors such as BMI can also still be trusted to indicate which individuals or groups are at risk of developing elevated LDL-c levels. Health advice should be given to appropriate target groups such as older women with a BMI >25kg/m2 in order to prevent CAD from becoming a burden in this population. / PhD (Dietetics), North-West University, Potchefstroom Campus, 2014
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The association of LDLR and PCSK9 variants with LDL-c levels in a black South African population in epidemiological transition / Tertia van ZylVan Zyl, Tertia January 2013 (has links)
Background
Elevated concentrations of low-density lipoprotein cholesterol (LDL-c) are a major risk factor for the development of coronary artery disease (CAD) because of their role in the progression of atherosclerosis. The black South African population is known to have had historically low LDL-c and in the past there was almost no CAD in the population. However, as this population moves through the nutrition transition, LDL-c levels are increasing. LDL-c levels are regulated by the LDL receptors, which is the major protein involved with transporting cholesterol across cell membranes in humans. Proprotein convertase subtilisinlike/kexin type 9 (PCSK9) is another protein involved with the regulation of LDL-c through its role in assisting with the degradation of the LDL receptor. Variants in both genes can cause elevated or lowered LDL-c levels. Very little information is available on the frequency or presence of variants in the low-density lipoprotein receptor (LDLR) and PCSK9 gene in the black South African population and on how these variants associate with LDL-c. The main aim of the study was thus to determine novel and existing genetic variants in these two genes and to describe the manner in which they associate with plasma LDL-c levels in a black South African population undergoing an epidemiological transition.
Methods
The 2005 baseline data from the Prospective Urban and Rural (PURE) study population were used in this study. The study population consisted of apparently healthy black volunteers form the North West province of South Africa, aged 35 to 60 years. Thirty individuals were randomly chosen from the 1860 volunteers to determine the presence of known and novel variants in these genes by automated bidirectional sequencing. The promoter region, exons and flanking regions were sequenced and variants were identified utilising CLC DNA Workbench. Deoxyribonucleic acid (DNA) samples for 1500 individuals of the PURE study population were genotyped by means of a Golden Gate Genotyping Assay. Analyses of covariance (ANCOVA) were used to test for associations between the different genotypes in both the LDLR and PCSK9 genes and LDL-c levels. Haplotypes were generated by using the confidence intervals on the software programme, HaploView. A genetic risk score (GRS) was determined by including variants which associated significantly with LDL-c. The GRS, the haplotypes and the variants that associated significantly with LDL-c were used in separate linear regression models with variants which correlated with LDL-c to determine how all these variables contribute to the differences in LDL-c levels.
Results and discussion
Novel and known variants were identified in both the genes and in total 52 variants were genotyped. Rare variants such as rs17249141 and rs28362286 were detected in the study population and are associated with low levels of LDL-c. The variants identified in the LDLR gene were situated largely in regulatory regions such as the promoter, intron and 3‟untranslated regions. Haplotypes in the LDLR gene with the highest frequency associated with lower LDL-c levels, which could contribute to the study population‟s low mean LDL-c level. Haplotypes identified in the PCSK9 gene had a weaker association with LDL-c levels. The minor allele frequencies of many of the variants differed from those of the European population and therefore the importance of population-specific research cannot be sufficiently emphasised. The GRS, haplotypes and variants used in the regression models to determine whether they contributed to predicting the variance in LDL-c in the study population made a small contribution to explaining this. BMI best explained the variance in LDL-c levels. Older women with a body mass index (BMI)>25kg/m2 were identified as being at greater risk of developing elevated LDL-c levels than the rest of the study population. Heterozygote carriers of variant, rs28362286, had 0.787 mmol/L lower LDL-c than carriers of the wild type and this is associated with a reduced risk of developing CAD.
Conclusion and recommendation
When considering the results mentioned above, adding genetic analysis to explaining the variance in LDL-c levels seems to have its limitations, but the study included only two of many genes that play a role in the metabolism and regulation of LDL-c levels. Incorporating more genes and more variants into analyses and prediction models will add greater value to defining LDL-c levels. Rarer variants with a large impact on protein function, such as rs28362286, have a greater effect on LDL-c levels and could predict the variance better than the common variants. Risk factors such as BMI can also still be trusted to indicate which individuals or groups are at risk of developing elevated LDL-c levels. Health advice should be given to appropriate target groups such as older women with a BMI >25kg/m2 in order to prevent CAD from becoming a burden in this population. / PhD (Dietetics), North-West University, Potchefstroom Campus, 2014
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Effect of Danazol on Plasma Lipid and Lipoprotein Levels in Normal WomenLuciano, Anthony A., Wallace, Robert B., Sherman, Barry M. 01 January 1982 (has links)
Prior studies of lipid and lipoprotein levels alterations associated with the administration of danazol, a testosterone derivative, in patients treated for endometriosis have been conflicting. We administered danazol to 7 normal menstruating women and measured plasma lipid and lipoprotein cholesterol levels prior to and 2 months after treatment. Small, non-significant decreases in total plasma cholesterol and triglyceride levels were seen, largely due to a dramatic decline in one woman with type IV hyperlipoproteinemia. No significant change in low density or very low density lipoprotein cholesterol levels was seen. However, a marked (40%) reduction of high density lipoprotein cholesterol level in the mean was found. These findings have implications for the atherogenic potential of danazol, the treatment of hyperlipidemia, and the relationship between gonadal hormones and lipoprotein levels.
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Meta-analysis and systematic review of the benefits expected when the glycaemic index is used in planning diets / Anna Margaretha OppermanOpperman, Anna Margaretha January 2004 (has links)
Motivation: The prevalence of non-communicable diseases such as diabetes mellitus (DM)
and cardiovascular disease (CVD) is rapidly increasing in industrialized societies. Experts
believe that lifestyle, and in particular its nutritional aspects, plays a decisive role in
increasing the burden of these chronic conditions. Dietary habits would, therefore, be
modified to exert a positive impact on the prevention and treatment of chronic diseases of
lifestyle. It is believed that the state of hyperglycaemia that is observed following food intake
under certain dietary regimes contributes to the development of various metabolic conditions.
This is not only true for individuals with poor glycaemic control such as some diabetics, but
could also be true for healthy individuals. It would, therefore, be helpful to be able to reduce
the amplitude and duration of postprandial hyperglycaemia. Selecting the correct type of
carbohydrate (CHO) foods may produce less postprandial hyperglycaemia, representing a
possible strategy in the prevention and treatment of chronic metabolic diseases. At the same
time, a key focus of sport nutrition is the optimal amount of CHO that an athlete should
consume and the optimal timing of consumption. The most important nutritional goals of the
athlete are to prepare body CHO stores pre-exercise, provide energy during prolonged
exercise and restore glycogen stores during the recovery period. The ultimate aim of these
strategies is to maintain CHO availability to the muscle and central nervous system during
prolonged moderate to high intensity exercise, since these are important factors in exercise
capacity and performance. However, the type of CHO has been studied less often and with
less attention to practical concerns than the amount of CHO.
The glycaemic index (GI) refers to the blood glucose raising potential of CHO foods and,
therefore, influences secretion of insulin. In several metabolic disorders, secretion of insulin
is inadequate or impossible, leading to poor glycaemic control. It has been suggested that
low GI diets could potentially contribute to a significant improvement of the conditions
associated with poor glycaemic control. Insulin secretion is also important to athletes since
the rate of glycogen synthesis depends on insulin due to it stimulatory effect on the activity of
glycogen synthase.
Objectives: Three main objectives were identified for this study. The first was to conduct a
meta-analysis of the effects of the GI on markers for CHO and lipid metabolism with the
emphasis on randomised controlled trials (RCT's). Secondly, a systematic review was
performed to determine the strength of the body of scientific evidence from epidemiological
studies combined with RCT's to encourage dieticians to incorporate the GI concept in meal
planning. Finally, a systematic review of the effect of the GI in sport performance was
conducted on all available literature up to date to investigate whether the application of the
GI in an athlete's diet can enhance physical performance.
Methodology: For the meta-analysis, the search was for randomised controlled trials with a
cross-over or parallel design published in English between 1981 and 2003, investigating the
effect of low GI vs high GI diets on markers of carbohydrate and lipid metabolism. The main
outcomes were serum fructosamine, glycosylated haemoglobin (HbA1c), high-density
lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), total cholesterol
(TC) and triacylglycerols (TG). For the systematic review, epidemiological studies as well as
RCT's investigating the effect of LGI vs HGI diets on markers for carbohydrate and lipid
metabolism were used. For the systematic review on the effect of the GI on sport
performance, RCT's with either a cross-over or parallel design that were published in English
between January 1981 and September 2004 were used. All relevant manuscripts for the
systematic reviews as well as meta-analysis were obtained through a literature search on
relevant databases such as the Cochrane Central Register of Controlled Trials, MEDLINE
(1981 to present), EMBASE, LILACS, SPORTDiscus, ScienceDirect and PubMed. This
thesis is presented in the article format.
Results and conclusions of the individual manuscripts:
For the meta-analysis, literature searches identified 16 studies that met the strict
inclusion criteria. Low GI diets significantly reduced fructosamine (p<0.05), HbA1c,
(p<0.03), TC(p<0.0001) and tended to reduce LDL-c (p=0.06) compared to high GI diets.
No changes were observed in HDL-c and TG concentrations. Results from this meta analysis,
therefore, support the use of the GI concept in choosing CHO-containing foods
to reduce TC and improve blood glucose control in diabetics.
The systematic review combined the results of the preceding meta-analysis and results
from epidemiological studies. Prospective epidemiological studies showed improvements
in HDL-c concentrations over longer time periods with low GI diets vs. high GI diets, while
the RCT's failed to show an improvement in HDL-c over the short-term. This could be
attributed to the short intervention period during which the RCT's were conducted.
Furthermore, epidemiological studies failed to show positive relationships between LDL-c
and TC and low GI diets, while RCT's reported positive results on both these lipids with
low GI diets. However, the epidemiological studies, as well as the RCT's showed positive
results with low GI diets on markers of CHO metabolism. Taken together, convincing
evidence from RCT's as well as epidemiological studies exists to recommend the use of
low GI diets to improve markers of CHO as well as of lipid metabolism.
3 From the systematic review regarding the GI and sport performance it does not seem that
low GI pre-exercise meals provide any advantages over high GI pre-exercise meals.
Although low GI pre-exercise meals may better maintain CHO availability during exercise,
low GI pre-exercise meals offer no added advantage over high GI meals regarding
performance. Furthermore, the exaggerated metabolic responses from high GI compared
to low GI CHO seems not be detrimental to exercise performance. However, athletes
who experience hypoglycaemia when consuming CHO-rich feedings in the hour prior to
exercise are advised to rather consume low GI pre-exercise meals. No studies have
been reported on the GI during exercise. Current evidence suggests a combination of
CHO with differing Gl's such as glucose (high GI), sucrose (moderate GI) and fructose
(low GI) will deliver the best results in terms of exogenous CHO oxidation due to different
transport mechanisms. Although no studies are conducted on the effect of the GI on
short-term recovery it is speculated that high GI CHO is most effective when the recovery
period is between 0-8 hours, however, evidence suggests that when the recovery period
is longer (20-24 hours), the total amount of CHO is more important than the type of CHO.
Conclusion: There is an important body of evidence in support of a therapeutic and
preventative potential of low GI diets to improve markers for CHO and lipid metabolism. By
substituting high GI CHO-rich with low GI CHO-rich foods improved overall metabolic control.
In addition, these diets reduced TC, tended to improve LDL-c and might have a positive
effect over the long term on HDL-c. This confirms the place for low GI diets in disease
prevention and management, particularly in populations characterised by already high
incidences of insulin resistance, glucose intolerance and abnormal lipid levels. For athletes it
seems that low GI pre-exercise meals do not provide any advantage regarding performance
over high GI pre-exercise meals. However, low GI meals can be recommended to athletes
who are prone to develop hypoglycaemia after a CHO-rich meal in the hour prior to exercise.
No studies have been reported on the effect of the GI during exercise. However, it has been
speculated that a combination of CHO with varying Gl's deliver the best results in terms of
exogenous CHO oxidation. No studies exist investigating the effect of the GI on short-term
recovery, however, it is speculated that high GI CHO-rich foods are suitable when the
recovery period is short (0-8 h), while the total amount rather than the type of CHO is
important when the recovery period is longer (20-24 h). Therefore, the GI is a scientifically
based tool to enable the selection of CHO-containing foods to improve markers for CHO and
lipid metabolism as well as to help athletes to prepare optimally for competitions.
Recommendations: Although a step nearer has been taken to confirm a place for the GI in
human health, additional randomised, controlled, medium and long-term studies as well as
more epidemiological studies are needed to investigate further the effect of low GI diets on
LDL-c. HDL-c and TG. These studies are essential to investigate the effect of low GI diets
on endpoints such as CVD and DM. This will also show whether low GI diets can reduce the
risk of diabetic complications such as neuropathy and nephropathy. Furthermore, the public
at large must be educated about the usefulness and application of the GI in meal planning.
For sport nutrition, randomised controlled trials should be performed to investigate the role of
the GI during exercise as well as in sports of longer duration such as cricket and tennis.
More studies are needed to elucidate the short-term effect of the GI post-exercise as well as
to determine the mechanism of lower glycogen storage with LGI meals post-exercise. / Thesis (Ph.D. (Dietetics))--North-West University, Potchefstroom Campus, 2005.
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Meta-analysis and systematic review of the benefits expected when the glycaemic index is used in planning diets / Anna Margaretha OppermanOpperman, Anna Margaretha January 2004 (has links)
Motivation: The prevalence of non-communicable diseases such as diabetes mellitus (DM)
and cardiovascular disease (CVD) is rapidly increasing in industrialized societies. Experts
believe that lifestyle, and in particular its nutritional aspects, plays a decisive role in
increasing the burden of these chronic conditions. Dietary habits would, therefore, be
modified to exert a positive impact on the prevention and treatment of chronic diseases of
lifestyle. It is believed that the state of hyperglycaemia that is observed following food intake
under certain dietary regimes contributes to the development of various metabolic conditions.
This is not only true for individuals with poor glycaemic control such as some diabetics, but
could also be true for healthy individuals. It would, therefore, be helpful to be able to reduce
the amplitude and duration of postprandial hyperglycaemia. Selecting the correct type of
carbohydrate (CHO) foods may produce less postprandial hyperglycaemia, representing a
possible strategy in the prevention and treatment of chronic metabolic diseases. At the same
time, a key focus of sport nutrition is the optimal amount of CHO that an athlete should
consume and the optimal timing of consumption. The most important nutritional goals of the
athlete are to prepare body CHO stores pre-exercise, provide energy during prolonged
exercise and restore glycogen stores during the recovery period. The ultimate aim of these
strategies is to maintain CHO availability to the muscle and central nervous system during
prolonged moderate to high intensity exercise, since these are important factors in exercise
capacity and performance. However, the type of CHO has been studied less often and with
less attention to practical concerns than the amount of CHO.
The glycaemic index (GI) refers to the blood glucose raising potential of CHO foods and,
therefore, influences secretion of insulin. In several metabolic disorders, secretion of insulin
is inadequate or impossible, leading to poor glycaemic control. It has been suggested that
low GI diets could potentially contribute to a significant improvement of the conditions
associated with poor glycaemic control. Insulin secretion is also important to athletes since
the rate of glycogen synthesis depends on insulin due to it stimulatory effect on the activity of
glycogen synthase.
Objectives: Three main objectives were identified for this study. The first was to conduct a
meta-analysis of the effects of the GI on markers for CHO and lipid metabolism with the
emphasis on randomised controlled trials (RCT's). Secondly, a systematic review was
performed to determine the strength of the body of scientific evidence from epidemiological
studies combined with RCT's to encourage dieticians to incorporate the GI concept in meal
planning. Finally, a systematic review of the effect of the GI in sport performance was
conducted on all available literature up to date to investigate whether the application of the
GI in an athlete's diet can enhance physical performance.
Methodology: For the meta-analysis, the search was for randomised controlled trials with a
cross-over or parallel design published in English between 1981 and 2003, investigating the
effect of low GI vs high GI diets on markers of carbohydrate and lipid metabolism. The main
outcomes were serum fructosamine, glycosylated haemoglobin (HbA1c), high-density
lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), total cholesterol
(TC) and triacylglycerols (TG). For the systematic review, epidemiological studies as well as
RCT's investigating the effect of LGI vs HGI diets on markers for carbohydrate and lipid
metabolism were used. For the systematic review on the effect of the GI on sport
performance, RCT's with either a cross-over or parallel design that were published in English
between January 1981 and September 2004 were used. All relevant manuscripts for the
systematic reviews as well as meta-analysis were obtained through a literature search on
relevant databases such as the Cochrane Central Register of Controlled Trials, MEDLINE
(1981 to present), EMBASE, LILACS, SPORTDiscus, ScienceDirect and PubMed. This
thesis is presented in the article format.
Results and conclusions of the individual manuscripts:
For the meta-analysis, literature searches identified 16 studies that met the strict
inclusion criteria. Low GI diets significantly reduced fructosamine (p<0.05), HbA1c,
(p<0.03), TC(p<0.0001) and tended to reduce LDL-c (p=0.06) compared to high GI diets.
No changes were observed in HDL-c and TG concentrations. Results from this meta analysis,
therefore, support the use of the GI concept in choosing CHO-containing foods
to reduce TC and improve blood glucose control in diabetics.
The systematic review combined the results of the preceding meta-analysis and results
from epidemiological studies. Prospective epidemiological studies showed improvements
in HDL-c concentrations over longer time periods with low GI diets vs. high GI diets, while
the RCT's failed to show an improvement in HDL-c over the short-term. This could be
attributed to the short intervention period during which the RCT's were conducted.
Furthermore, epidemiological studies failed to show positive relationships between LDL-c
and TC and low GI diets, while RCT's reported positive results on both these lipids with
low GI diets. However, the epidemiological studies, as well as the RCT's showed positive
results with low GI diets on markers of CHO metabolism. Taken together, convincing
evidence from RCT's as well as epidemiological studies exists to recommend the use of
low GI diets to improve markers of CHO as well as of lipid metabolism.
3 From the systematic review regarding the GI and sport performance it does not seem that
low GI pre-exercise meals provide any advantages over high GI pre-exercise meals.
Although low GI pre-exercise meals may better maintain CHO availability during exercise,
low GI pre-exercise meals offer no added advantage over high GI meals regarding
performance. Furthermore, the exaggerated metabolic responses from high GI compared
to low GI CHO seems not be detrimental to exercise performance. However, athletes
who experience hypoglycaemia when consuming CHO-rich feedings in the hour prior to
exercise are advised to rather consume low GI pre-exercise meals. No studies have
been reported on the GI during exercise. Current evidence suggests a combination of
CHO with differing Gl's such as glucose (high GI), sucrose (moderate GI) and fructose
(low GI) will deliver the best results in terms of exogenous CHO oxidation due to different
transport mechanisms. Although no studies are conducted on the effect of the GI on
short-term recovery it is speculated that high GI CHO is most effective when the recovery
period is between 0-8 hours, however, evidence suggests that when the recovery period
is longer (20-24 hours), the total amount of CHO is more important than the type of CHO.
Conclusion: There is an important body of evidence in support of a therapeutic and
preventative potential of low GI diets to improve markers for CHO and lipid metabolism. By
substituting high GI CHO-rich with low GI CHO-rich foods improved overall metabolic control.
In addition, these diets reduced TC, tended to improve LDL-c and might have a positive
effect over the long term on HDL-c. This confirms the place for low GI diets in disease
prevention and management, particularly in populations characterised by already high
incidences of insulin resistance, glucose intolerance and abnormal lipid levels. For athletes it
seems that low GI pre-exercise meals do not provide any advantage regarding performance
over high GI pre-exercise meals. However, low GI meals can be recommended to athletes
who are prone to develop hypoglycaemia after a CHO-rich meal in the hour prior to exercise.
No studies have been reported on the effect of the GI during exercise. However, it has been
speculated that a combination of CHO with varying Gl's deliver the best results in terms of
exogenous CHO oxidation. No studies exist investigating the effect of the GI on short-term
recovery, however, it is speculated that high GI CHO-rich foods are suitable when the
recovery period is short (0-8 h), while the total amount rather than the type of CHO is
important when the recovery period is longer (20-24 h). Therefore, the GI is a scientifically
based tool to enable the selection of CHO-containing foods to improve markers for CHO and
lipid metabolism as well as to help athletes to prepare optimally for competitions.
Recommendations: Although a step nearer has been taken to confirm a place for the GI in
human health, additional randomised, controlled, medium and long-term studies as well as
more epidemiological studies are needed to investigate further the effect of low GI diets on
LDL-c. HDL-c and TG. These studies are essential to investigate the effect of low GI diets
on endpoints such as CVD and DM. This will also show whether low GI diets can reduce the
risk of diabetic complications such as neuropathy and nephropathy. Furthermore, the public
at large must be educated about the usefulness and application of the GI in meal planning.
For sport nutrition, randomised controlled trials should be performed to investigate the role of
the GI during exercise as well as in sports of longer duration such as cricket and tennis.
More studies are needed to elucidate the short-term effect of the GI post-exercise as well as
to determine the mechanism of lower glycogen storage with LGI meals post-exercise. / Thesis (Ph.D. (Dietetics))--North-West University, Potchefstroom Campus, 2005.
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Serum High Sensitivity C-Reactive Protein, White Blood Cell Count, and High-Density Lipoprotein Cholesterol Levels are Associated with Coronary Artery Lesions in Kawasaki DiseaseOu, Chum-yen 04 July 2007 (has links)
Background: Kawasaki disease (KD) affects mainly children younger than five years of age, leading to coronary artery lesions, and even to life-threatening myocardial infarctions. Since 1976, Kawasaki disease has occurred among thousands of children in Taiwan. Evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. Significant determinants of high sensitivity C-reactive protein (hs-CRP), which is a sensitive indicator of inflammation, as well as white blood cell (WBC) count, and high-density lipoprotein cholesterol (HDLc) and coronary artery lesion were identified. The relationships between these factors¡¦ concentration and arterial lesion were likewise investigated and had reported. The aim of this study was to determine the serum levels of the hs-CRP, WBC count, and plasma HDLc levels in patients with later phase of KD.
Methods and Materials: From July 2005 to June 2006, 97 children with Kawasaki disease at least 1 year after diagnosis were recruited in this study. These participated children had been diagnosed as KD and collected at the interval of 2001 to 2004. Diagnosis was based on the 1984 revised by the KD Research Committee in Japan. The participants were grouped into 45 patients with KD and coronary aneurysms (Group I), 52 patients with KD and normal coronary arteries (Group II), and 50 healthy age-matched children (Control Group III). Their WBC count, systemic and diastolic blood pressures, body mass index, age, sex, fasting total cholesterol concentrations, triglyceride, high-density lipoprotein cholesterol (HDLc), low-density lipoprotein cholesterol, serum hs-CRP levels, and coronary artery lesion by cardioechography were recorded and compared. The analytical differences between hs-CRP, WBC count, and plasma HDLc levels and the coronary artery events in KD were examined.
Results: Serum hs-CRP levels of Group I patients (mean 0.264 mg/dl) was significantly greater than that of Group II (mean 0.155 mg/dl, p=0.006) and Group III patients (mean 0.116 mg/dl, p =0.017). Similarly, the WBC count of Group I patients (mean 6,543.11/mm3) was significantly greater than that of Group II (mean 5,720.19/mm3, p=0.029), and Group III patients (mean 5,611.27/mm3, p =0.012). However, plasma HDLc levels of Group I patients (mean 41.42 mg/dl) was significantly lesser than that of Group II (mean 44.79 mg/dl, p=0.035), and Control Group III patients (mean 46.58 mg/dl, p=0.027). There was a positive association between hs-CRP and WBC count levels (r = 0.641, p < 0.05), but none between hs-CRP and plasma HDLc levels.
Conclusions: There is the possibility of ongoing low-grade inflammation late after the convalescent phase of Kawasaki disease in children with coronary aneurysms, which may have a role in increasing coronary artery dysfunction. These results also suggest that hs-CRP, WBC count, and plasma HDLc levels are useful parameters for predicting formation of coronary artery lesion even in children after onset of KD.
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What are the effects of lowering LDL-cholesterol on risk of stroke in chronic kidney disease? : evidence from the Study of Heart and Renal Protection (SHARP)Herrington, William Guy January 2013 (has links)
No description available.
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Hypobetalipoproteinaemia and truncated forms of human apolipoprotein BMcCormick, Sally Priscilla Anna January 1992 (has links)
A new variant of human apolipoprotein B has been identified in a subject with decreased low density lipoprotein cholesterol and apolipoprotein B concentrations. Although no clinical signs of fat malabsorption were observed the subject was diagnosed, on the basis of his low cholesterol and apolipoprotein B level, as having hypobetalipoproteinaemia. The variant of apolipoprotein B was first identified by Western blot analysis. The analysis revealed an abnormal low molecular weight form of apolipoprotein B as well as normal apolipoprotein B-100 indicating that the subject was heterozygous for a truncated form of apolipoprotein B. The new variant (apo B-32) was a result of a C→T transition at nucleotide 4548 in exon 26 of the apolipoprotein B gene. This mutation changes a CAG codon which codes for glutamine into a TAG stop codon resulting in translation of a truncated apolipoprotein B protein approximately 32% the length of normal apolipoprotein B-100. Although only 32% of the length of apolipoprotein B-100, apo B-32 was still capable of forming lipoprotein particles as indicated by its presence in both the low density and high density lipoprotein fractions. This density distribution is unique since apo B-32 is the shortest known truncated apolipoprotein B to be found in the low density lipoprotein fraction. This finding clearly indicates that the region of apo B-32 is important in the lipid binding characteristics of apolipoprotein B-100. The binding of apo B-32 to heparin confirmed three heparin binding sites previously predicted to be in the amino-terminal 30% of apolipoprotein B-100. Isolated lipoproteins formed from apo B-32 appeared to be similar to high density lipoproteins in size and composition. However, unlike high density lipoproteins, the apo B-32 lipoproteins in plasma were partially precipitated by polyanionlcation reagents normally used to precipitate very low density and low density lipoproteins. The presence of both apolipoproteins Al and E on the apo B-32 lipoproteins suggested that apolipoprotein Al or E may mediate the metabolism of apo B-32 since apo B-32 does not posses the receptor binding region for the low density lipoprotein receptor. Four further subjects were identified as having reduced low density lipoprotein and apolipoprotein B concentrations. However a lack of any truncated apolipoprotein B in their plasma made it difficult to link their hypobetalipoproteinaemia with the apolipoprotein B gene. The cause of the hypobetalipoproteinaemia in these subjects remains uncharacterised although future linkage analysis studies in these individuals and family members will at least establish whether their hypobetalipoproteinaemia is related to the apo B gene.
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