Dietary Oxidized Lipids Affect Phospholipid Profile and Fatty Acid Uptake in Gastrointestinal Cells

Obesity and hyperlipidemia are the most prevalent independent risk factors of chronic kidney disease (CKD), suggesting that lipid accumulation in the renal parenchyma is detrimental to renal function. Non-esterified fatty acids (also known as free fatty acids, FFA) are especially harmful to the kidneys. A concerted, increased FFA uptake due to high fat diets, overexpression of fatty acid uptake systems such as the CD36 scavenger receptor and the fatty acid transport proteins, and a reduced β-oxidation rate underlie the intracellular lipid accumulation in non-adipose tissues. FFAs in excess can damage podocytes, proximal tubular epithelial cells and the tubulointerstitial tissue through various mechanisms, in particular by boosting the production of reactive oxygen species (ROS) and lipid peroxidation, promoting mitochondrial damage and tissue inflammation, which result in glomerular and tubular lesions. Not all lipids are bad for the kidneys: polyunsaturated fatty acids (PUFA) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) seem to help lag the progression of chronic kidney disease (CKD). Lifestyle interventions, especially dietary adjustments, and lipid-lowering drugs can contribute to improve the clinical outcome of patients with CKD.

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Effect of insulin on free fatty acid uptake by hepatocytes in the duck

Journal of Endocrinology ◽

10.1677/joe.0.1020381 ◽

1984 ◽

Vol 102 (3) ◽

pp. 381-386 ◽

Cited By ~ 4

Author(s):

R. Gross ◽

P. Mialhe

Keyword(s):

Fatty Acids ◽

Growth Hormone ◽

Fatty Acid ◽

Free Fatty Acid ◽

Glucose Metabolism ◽

Free Fatty Acids ◽

Fatty Acid Uptake ◽

Acid Uptake ◽

Low Doses ◽

Higher Doses

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386

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Isotope tracer measures of meal fatty acid metabolism: reproducibility and effects of the menstrual cycle

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00340.2004 ◽

2005 ◽

Vol 288 (3) ◽

pp. E547-E555 ◽

Cited By ~ 44

Author(s):

Ana Paola Uranga ◽

James Levine ◽

Michael Jensen

Keyword(s):

Fatty Acids ◽

Adipose Tissue ◽

Fatty Acid ◽

Menstrual Cycle ◽

Dietary Fat ◽

Fatty Acid Uptake ◽

Upper Body ◽

Acid Oxidation ◽

Acid Uptake ◽

Lower Body

Oxidation and adipose tissue uptake of dietary fat can be measured by adding fatty acid tracers to meals. These studies were conducted to measure between-study variability of these types of experiments and assess whether dietary fatty acids are handled differently in the follicular vs. luteal phase of the menstrual cycle. Healthy normal-weight men ( n = 12) and women ( n = 12) participated in these studies, which were block randomized to control for study order, isotope ([3H]triolein vs. [14C]triolein), and menstrual cycle. Energy expenditure (indirect calorimetry), meal fatty acid oxidation, and meal fatty acid uptake into upper body and lower body subcutaneous fat (biopsies) 24 h after the experimental meal were measured. A greater portion of meal fatty acids was stored in upper body subcutaneous adipose tissue (24 ± 2 vs. 16 ± 2%, P < 0.005) and lower body fat (12 ± 1 vs. 7 ± 1%, P < 0.005) in women than in men. Meal fatty acid oxidation (3H2O generation) was greater in men than in women (52 ± 3 vs. 45 ± 2%, P = 0.04). Leg adipose tissue uptake of meal fatty acids was 15 ± 2% in the follicular phase of the menstrual cycle and 10 ± 1% in the luteal phase ( P = NS). Variance in meal fatty acid uptake was somewhat ( P = NS) greater in women than in men, although menstrual cycle factors did not contribute significantly. We conclude that leg uptake of dietary fat is slightly more variable in women than in men, but that there are no major effects of menstrual cycle on meal fatty acid disposal.

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AMPK-mediated increase in myocardial long-chain fatty acid uptake critically depends on sarcolemmal CD36

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2007.01.141 ◽

2007 ◽

Vol 355 (1) ◽

pp. 204-210 ◽

Cited By ~ 88

Author(s):

Daphna D.J. Habets ◽

Will A. Coumans ◽

Peter J. Voshol ◽

Marion A.M. den Boer ◽

Maria Febbraio ◽

...

Keyword(s):

Fatty Acid ◽

Fatty Acid Uptake ◽

Chain Fatty Acid ◽

Acid Uptake ◽

Long Chain Fatty Acid ◽

Long Chain

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The effect of high glucose on lipid metabolism in the human placenta

Scientific Reports ◽

10.1038/s41598-019-50626-x ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 5

Author(s):

Charlotte H. Hulme ◽

Anna Nicolaou ◽

Sharon A. Murphy ◽

Alexander E. P. Heazell ◽

Jenny E. Myers ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

High Glucose ◽

Fatty Acid Uptake ◽

Fatty Acid Transport ◽

Acid Uptake ◽

Obese Women ◽

Lipid Transfer ◽

Glucose Levels ◽

Fatty Acid Transport Proteins

Abstract Diabetes mellitus (DM) during pregnancy can result in fetal overgrowth, likely due to placental dysfunction, which has health consequences for the infant. Here we test our prediction from previous work using a placental cell line that high glucose concentrations affect placental lipid metabolism. Placentas from women with type 1 (n = 13), type 2 (n = 6) or gestational (n = 12) DM, BMI-matched to mothers without DM (n = 18), were analysed for lipase and fatty acid transport proteins and fatty acid and triglyceride content. Explants from uncomplicated pregnancies (n = 6) cultured in physiological or high glucose were similarly analysed. High glucose levels did not alter placental lipase or transporter expression or the profile and abundance of fatty acids, but triglyceride levels were higher (p < 0.05), suggesting reduced β- oxidation. DM did not affect placental protein expression or fatty acid profile. Triglyceride levels of placentas from mothers with pre-existing DM were similar to controls, but higher in obese women with gestational DM. Maternal hyperglycemia may not affect placental fatty acid uptake and transport. However, placental β-oxidation is affected by high glucose and reduced in a subset of women with DM. Abnormal placental lipid metabolism could contribute to increased maternal-fetal lipid transfer and excess fetal growth in some DM pregnancies.

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