Plasma Lipid and Lipoprotein Abnormalities in Patients with Malabsorption

1973 ◽  
Vol 45 (5) ◽  
pp. 583-592 ◽  
Author(s):  
Gilbert R. Thompson ◽  
J. Paul Miller
Keyword(s):  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Serum Triglyceride ◽  
Plasma Lipoproteins ◽  
Low Density ◽  
Cholesterol Levels ◽  
Lipids And Lipoproteins

1. Plasma lipids and lipoproteins have been studied in control subjects and patients with various types of steatorrhoea. 2. Low plasma cholesterol levels were found in malabsorbers and were associated with decreased amounts of low-density lipoprotein (LDL) in males and high-density lipoprotein (HDL) in females. 3. Serum triglyceride levels were normal in males, but exceeded control values in some of the females, due to an increase in very-low-density lipoprotein. 4. LDL composition was abnormal in both male and female malabsorbers, with a decreased proportion of cholesterol ester and an increased proportion of triglyceride. There was also an increased proportion of triglyceride in HDL. 5. These findings show that malabsorption markedly influences not only the concentration but also the composition of plasma lipoproteins.

scholarly journals (Pro)renin Receptor Inhibition Reduces Plasma Cholesterol and Triglycerides but Does Not Attenuate Atherosclerosis in Atherosclerotic Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Dien Ye ◽  
Xiaofei Yang ◽  
Liwei Ren ◽  
Hong S. Lu ◽  
Yuan Sun ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Inflammatory Responses ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Low Density ◽  
Beneficial Effects ◽  
Receptor Inhibition ◽  
Density Lipoprotein Receptor

Objective: Elevated plasma cholesterol concentrations contributes to ischemic cardiovascular diseases. Recently, we showed that inhibiting hepatic (pro)renin receptor [(P)RR] attenuated diet-induced hypercholesterolemia and hypertriglyceridemia in low-density lipoprotein receptor (LDLR) deficient mice. The purpose of this study was to determine whether inhibiting hepatic (P)RR could attenuate atherosclerosis.Approach and Results: Eight-week-old male LDLR−/− mice were injected with either saline or N-acetylgalactosamine-modified antisense oligonucleotides (G-ASOs) primarily targeting hepatic (P)RR and were fed a western-type diet (WTD) for 16 weeks. (P)RR G-ASOs markedly reduced plasma cholesterol concentrations from 2,211 ± 146 to 1,128 ± 121 mg/dL. Fast protein liquid chromatography (FPLC) analyses revealed that cholesterol in very low-density lipoprotein (VLDL) and intermediate density lipoprotein (IDL)/LDL fraction were potently reduced by (P)RR G-ASOs. Moreover, (P)RR G-ASOs reduced plasma triglyceride concentrations by more than 80%. Strikingly, despite marked reduction in plasma lipid concentrations, atherosclerosis was not reduced but rather increased in these mice. Further testing in ApoE−/− mice confirmed that (P)RR G-ASOs reduced plasma lipid concentrations but not atherosclerosis. Transcriptomic analysis of the aortas revealed that (P)RR G-ASOs induced the expression of the genes involved in immune responses and inflammation. Further investigation revealed that (P)RR G-ASOs also inhibited (P)RR in macrophages and in enhanced inflammatory responses to exogenous stimuli. Moreover, deleting the (P)RR in macrophages resulted in accelerated atherosclerosis in WTD fed ApoE−/− mice.Conclusion: (P)RR G-ASOs reduced the plasma lipids in atherosclerotic mice due to hepatic (P)RR deficiency. However, augmented pro-inflammatory responses in macrophages due to (P)RR downregulation counteracted the beneficial effects of lowered plasma lipid concentrations on atherosclerosis. Our study demonstrated that hepatic (P)RR and macrophage (P)RR played a counteracting role in atherosclerosis.

Plasma lipids, lipoproteins, and triglyceride turnover in eu- and hypo-thyroid rats and rats on a hypocaloric diet

1981 ◽  
Vol 59 (8) ◽  
pp. 715-721 ◽  
Author(s):  
Ladislav Dory ◽  
Brian R. Krause ◽  
Paul S. Roheim
Keyword(s):  
Half Life ◽  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Caloric Intake ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Plasma Triglyceride ◽  
Low Density ◽  
Control Groups

Lipid and lipoprotein concentration, and triglyceride turnover were studied in control, thyroidectomized, and pair-fed control rats (pair-fed to match the food intake of the thyroidectomized rats). Thyroidectomy induced a significant increase in plasma cholesterol (and low density lipoprotein) concentrations and a decrease in plasma triglyceride (and very low density lipoprotein) concentrations. Changes in similar direction but of smaller magnitude were observed in the plasma of the pair-fed control rats. To further investigate triglyceride metabolism in these three groups of animals, triglyceride turnover was studied in fasted, unrestrained, and unanesthetized rats, following injection of [2-3H]glycerol. Peak incorporation of [2-3H]glycerol into plasma triglyceride occurred in all three groups of animals at 25 min after precursor administration, although the maximal incorporation was substantially lower in the thyroidectomized group than in either of the control groups. Thereafter, plasma triglyceride radioactivity decayed monoexponentially with a half-life of 24 ± 1 min for both normal and pair-fed control rats, compared with the half-life of 41 ± 3 min observed in the thyroidectomized rats. The calculated apparent fractional catabolic rates were thus 0.029 min−1 for both control groups and only 0.017 min−1 for the thyroidectomized animals. The apparent total catabolic rates of plasma triglyceride were 299 ± 11, 138 ± 11, and 48 ± 4 μg triglyceride∙min−1 for the normal controls, pair-fed controls, and thyroidectomized rats, respectively. These data further emphasize the importance of thyroid hormones in regulating plasma lipid and lipoprotein metabolism and, specifically, indicate that hypothyroidism results in a reduction of triglyceride secretion into, and the removal from, circulation. Furthermore, evidence was presented that the decreased caloric intake of the hypothyroid animals cannot, in itself, account for this observation.

scholarly journals An Overview on Hyperlipidemia

2021 ◽  
pp. 543-555
Author(s):  
D. A. Helen Sheeba ◽  
R. Gandhimathi
Keyword(s):  
Plasma Lipids ◽  
Medical Condition ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Research Work ◽  
Density Lipoprotein ◽  
High Plasma ◽  
Plasma Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density

Introduction: Hyperlipidemia is a medical condition indicated by an increase in one or more plasma lipids, such as triglycerides, cholesterol, cholesterol esters, phospholipids, and/or plasma lipoproteins, such as very low-density lipoprotein and low-density lipoprotein, as well as decreased levels of high-density lipoprotein. This increase in plasma lipids is one of the most important risk factors for cardiovascular disease. In the meanwhile, statins and fibrates remain the most common anti-hyperlipidemic drugs for treating high plasma cholesterol and triglycerides. Conclusion: Hence this review focused to study of hyperlipidemia. This review is useful to research work in hyperlididemia.

scholarly journals Loss of TIMP4 (Tissue Inhibitor of Metalloproteinase 4) Promotes Atherosclerotic Plaque Deposition in the Abdominal Aorta Despite Suppressed Plasma Cholesterol Levels

2021 ◽  
Author(s):  
Mei Hu ◽  
Sayantan Jana ◽  
Tolga Kilic ◽  
Faqi Wang ◽  
Mengcheng Shen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Thoracic Aorta ◽  
Abdominal Aorta ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Plaque Deposition ◽  
Cholesterol Levels

Objective: Atherosclerosis is accumulation of lipids and extracellular matrix in the arterial wall. TIMPs (tissue inhibitor of metalloproteinases) can impact plaque deposition by regulating ECM (extracellular matrix) turnover. TIMP4 also influences lipid metabolism and smooth muscle cell (SMC) proliferation. We investigated the role of TIMP4 in atherosclerosis. Approach and Results: Mice lacking low-density lipoprotein receptor ( Ldlr −/− ) and Timp4 ( Timp4 −/− / Ldlr −/− ) were fed high-fat diet (HFD) or regular laboratory diet. After 3 or 6 months, HFD-fed male and female Timp4 −/− / Ldlr −/− mice exhibited higher plaque density in the abdominal aorta (but not in aortic valves, arch, thoracic aorta) compared with Ldlr −/− mice. Although plasma lipid and cholesterol levels were lower in Timp4 −/− / Ldlr −/− -HFD, cholesterol content in the abdominal aorta was higher along with elevated inflammatory cytokines, MMP (matrix metalloproteinase) activities, CD68 + /calponin + macrophage-like SMCs in Timp4 −/− / Ldlr −/− -HFD compared with Ldlr −/− -HFD mice. In vitro, oxidized LDL (low-density lipoprotein) markedly increased CD68 expression, reduced SMC markers, increased lipid uptake, and reduced cholesterol efflux protein ABCA1 (ATP-binding cassette transporter A1) in Timp4 −/− / Ldlr −/− compared with Ldlr −/− primary SMCs from abdominal, but not thoracic aorta. TIMP4 expression in the abdominal aorta (in vivo) and its corresponding SMCs (in vitro) was ≈2-fold higher than in the thoracic aorta and SMCs; TIMP4 levels decreased following HFD. Timp4 -deficiency in bone marrow–derived macrophages did not alter their foam cell formation capacity. Conclusions: TIMP4 protects against plaque deposition in the abdominal aorta independent of plasma cholesterol levels. TIMP4 prevents proteolytic degradation of ABCA1 in SMCs, hindering cholesterol accumulation and transdifferentiation to macrophage-like foam cells, representing a novel negative regulator of atherosclerosis.

A Longitudinal Genetic Study of Plasma Lipids in Adolescent Twins

2007 ◽  
Vol 10 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Rita P. S. Middelberg ◽  
Nicholas G. Martin ◽  
John B. Whitfield
Keyword(s):  
Total Cholesterol ◽  
Environmental Effects ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Environmental Influences ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Lipids And Lipoproteins ◽  
Adolescent Twins ◽  
Over Time

AbstractPlasma lipids such as high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol and triglyceride levels contribute to variation in the risk of cardiovascular disease. The early stages of atherosclerosis in childhood have also been associated with changes in triglycerides, LDL and HDL. Heritability estimates for lipids and lipoproteins for adolescents are in the range .71 to .82, but little is known about changes of genetic and environmental influences over time in adolescence. We have investigated the contribution of genetic and environmental influences to variation in lipids in adolescent twins and their nontwin siblings using longitudinal twin and family data. Plasma HDL and LDL cholesterol, total cholesterol and triglycerides data from 965 twin pairs at 12, 14 and 16 years of age and their siblings have been analyzed. Longitudinal genetic models that included effects of age, sex and their interaction were fitted to assess whether the same or different genes influence each trait at different ages. Results suggested that more than one genetic factor influences HDL, LDL, total cholesterol and triglycerides over time at ages 12, 14 and 16 years. There was no evidence of shared environmental effects except for HDL and little evidence of long-term nonshared environmental effects was found. Our study suggested that there are developmental changes in the genes affecting plasma lipid concentrations across adolescence.

ARH missense polymorphisms and plasma cholesterol levels

2004 ◽  
Vol 42 (9) ◽  
Author(s):  
Jaroslav A. Hubacek ◽  
Tommy Hyatt
Keyword(s):  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Adaptor Protein ◽  
Low Density ◽  
Cholesterol Levels

AbstractMutations in a putative low-density lipoprotein (LDL) receptor adaptor protein called

Implications of decreased serum adiponectin for type IIb hyperlipidaemia and increased cholesterol levels of very-low-density lipoprotein in type II diabetic patients

2005 ◽  
Vol 109 (3) ◽  
pp. 297-302 ◽  
Author(s):  
Hiroshi Yoshida ◽  
Yuji Hirowatari ◽  
Hideo Kurosawa ◽  
Norio Tada
Keyword(s):  
Gender Difference ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Serum Adiponectin ◽  
Diabetic Patients ◽  
Low Density ◽  
Type Ii ◽  
Cholesterol Levels ◽  
Vldl Cholesterol

The present study was performed to investigate the relevance of cholesterol levels of plasma lipoproteins [HDL (high-density lipoprotein), LDL (low-density lipoprotein), IDL (immediate-density lipoprotein), VLDL (very-LDL) and chylomicrons] determined by a novel HPLC method, with adiponectin, which is decreased in Type II diabetes and assumed to be involved in dysregulated metabolism and atherogenesis. Type II diabetic patients who were not treated with insulin, statins and fibrates were enrolled. Study subjects included Type II diabetic patients with normolipidaemia (DM-NL; n=15), type 4 hyperlipidaemia (DM-T4HL; n=13), Type IIa hyperlipidaemia (DM-T2aHL; n=15) and Type IIb hyperlipidaemia (DM-T2bHL; n=13). Fasting blood samples were collected. The serum adiponectin level was lower in DM-T2bHL than in any of the other groups. Cholesterol levels of each lipoprotein fraction, serum triacylglycerol (triglyceride), remnant-like particle-cholesterol, fasting plasma glucose, HbA1c (glycated haemoglobin), age, gender difference and BMI (body mass index) were incorporated into a stepwise regression analysis as independent variables. VLDL-cholesterol correlated inversely with adiponectin independently of age, BMI, gender difference and glycaemic control. Although the mechanisms remain to be explored, serum adiponectin was reduced particularly in Type II diabetics with type IIb hyperlipidaemia and correlated inversely with VLDL-cholesterol. Measuring VLDL-cholesterol may be helpful for understanding the pathological features of diabetic dyslipidaemia.

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