Sentences with phrase «ldl receptor»

His key observation is that thyroid hormone stimulates expression of the LDL receptor (1).

I'll be posting on this soon, but here's the gist of it: High LDL on low - carb Paleo is due to a combination of being too low - carb (which reduces thyroid hormone and LDL receptor activity) and oxidative stress (usually due to a lack of antioxidant minerals: zinc, copper, selenium), possibly compounded by hypothyroidism (usually due to infection or to selenium or iodine deficiencies).

I have a strong family history and suspect LDL receptor insufficiency.

Some say its a numbers game, the more LDL particles crashing the walls of the arteries... some say the LDL is only a sign of vascular damage, but if my LDL goes down on a low fat diet, then that is bs, some say that it may be a problem metabolizing LDL, intake / production is outpacing LDL receptor activity, some say its not LDL but LDL that stays in the blood too long and oxidizes, some say about 20 % carbs (I was less than 5 %) will produce just enough insulin to help metabolize cholesterol, but the hard core low carb guys, say the whole cholesterol thing is a scam and cholesterol under 500, without insulin resistance is nothing to worry about.

Low thyroid function leads to poor expression of the LDL receptor and increased cholesterol production by the body (10).

His parenthetical remark indicates that the Nobel prize was awarded for the discovery of the LDL receptor and its associated pathway, not for the statement about saturated fats.

No one to my knowledge has shown that this is due to reduced LDL receptor activity.

Not «blocking» the LDL receptor.

«My research group and I believe that the high amounts of dietary saturated fats in the western diet promote atherosclerosis because they down - regulate the LDL receptor (a concept for which the Nobel prize in medicine was awarded in 1984).

The whole reason we care about the LDL receptor is that if LDL is not cleared from the blood in a timely fashion it will oxidize!

Second, the role of the LDL receptor in health and of cholesterol in regulating that receptor.

poor LDL receptor actiity is often signified by poor Total to HDL ratio and small dense LDL particles which could be why these two markers have appeared predictive.

«[H] igh LDL receptor content in human breast cancer tissue seems to indicate a poor prognosis, suggest [ing] that breast tumours rich in LDL receptors may grow rapidly» in the body.

Their discovery of the LDL receptor as the major molecule regulating cholesterol metabolism and its genetic disruption in the human disease familial hypercholesterolemia have been recognized by their receipt of numerous awards, including the Nobel Prize in Physiology or Medicine (1985), the Albert D. Lasker Award in Basic Medical Research (1985), and the U.S. National Medal of Science (1988).

Abbreviations: ASC, apoptosis - associated speck - like protein containing a caspase - recruitment domain; ATM, adipose - tissue - resident macrophage; BAT, brown adipose tissue; CCR2, CC chemokine receptor 2; CHOP, C / EBP (CCAAT / enhancer - binding protein)- homologous protein; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; GPCR, G - protein - coupled receptor; HIF, hypoxia - inducible factor; IFNγ, interferon γ; IKK, inhibitor of nuclear factor κB kinase; IL, interleukin; IRS - 1, insulin receptor substrate - 1; JNK, c - Jun N - terminal kinase; LDL, low - density lipoprotein; Ldlr, LDL receptor; LXR, liver X receptor; MCP - 1, monocyte chemoattractant protein 1; miRNA, microRNA; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NF - κB, nuclear factor κB; NLRP3, NLR (nucleotide - binding - domain - and leucine - rich - repeat - containing) family, pyrin - domain - containing 3; oxLDL, oxidized LDL; PKR, double - stranded RNA - dependent protein kinase; PPAR, peroxisome - proliferator - activated receptor; STAT6, signal transducer and activator of transcription 6; SVF, stromal vascular fraction; TLR, Toll - like receptor; TNFα, tumour necrosis factor α; UPR, unfolded protein response; WAT, white adipose tissue

Subramanian S, Goodspeed L, Wang S, Kim J, Zeng L, Ioannou GN, Haigh WG, Yeh MM, Kowdley KV, O'Brien KD, Pennathur S, Chait A. Dietary cholesterol exacerbates hepatic steatosis and inflammation in obese LDL receptor - deficient mice.

Walenbergh SMA, Houben T, Hendrikx T, Jeurissen MLJ, Gorp van PJ, Vaes N, Olde Damink SWM, Verheyen F, Koek GH, Lütjohann D, Grebe A, Latz E, Shiri - Sverdlov R. Weekly Treatment of 2 - Hydroxypropyl - β - cyclodextrin Improves Intracellular Cholesterol Levels in LDL Receptor Knockout Mice.

If PCSK9 is blocked, the LDL receptor is recycled back into the cell membrane and can remove additional LDL particles from the extracellular fluid.

Furthermore, enhanced hiPS - HEP cells express high levels of the LDL receptor (Figure 5, Panel B) and take up fluorescently labeled LDL (Figure 5, Panel A).

Cholesterol - induced hepatic inflammation does not underlie the predisposition to insulin resistance in dyslipidemic female LDL receptor knockout mice.

Abbreviations: LDLR = LDL receptor; APOB / A1 = apolipoprotein B - 100 / A1; PCSK9 = proprotein convertase subtilisin / kexin type 9; SREBP - 1 / 2 = sterol regulatory element - binding protein 1/2; LPL = lipoprotein lipase; FATP2 / 4/5 = fatty acid transporter protein 2 / 4/5; FASN = fatty acid synthase; SCD5 = stearoyl - CoA desaturase 5; ACADL = acyl - CoA dehydrogenase; L - FABP = liver fatty acid - binding protein; and CPT1A = carnitine O - palmitoyltransferase 1.

The plasma concentrations of apoproteins B - 100 and E, the two ligands for the LDL receptor, declined by more than 90 percent after cadmium treatment, but the concentration of another apoprotein, A-I, was unaffected.

Cloning and sequencing of complementary DNA's from normal and WHHL rabbits, shows that this defect arises from an in - frame deletion of 12 nucleotides that eliminates four amino acids from the cysteine - rich ligand binding domain of the LDL receptor.

Deletion in cysteine - rich region of LDL receptor impedes transport to cell surface in WHHL rabbit

A similar mutation, detected by S1 nuclease mapping of LDL receptor messenger RNA, occurred in a patient with familial hypercholesterolemia whose receptor also fails to be transported to the cell surface.

A line of transgenic mice was studied that express the human LDL receptor gene in the liver under control of the transferrin promoter.

Their discovery of the LDL receptor and their efforts to understand how the protein functioned are credited with laying the foundation for the development of the blockbuster class of cholesterol - lowering statin drugs.

This finding suggests that the homologous region may have resulted from a duplication of an ancestral gene and that the two genes evolved further by recruitment of exons from other genes, which provided the specific functional domains of the LDL receptor and the EGF precursor.

A complementary DNA encoding the human low density lipoprotein (LDL) receptor under control of the mouse metallothionein - I promoter was injected into fertilized mouse eggs, and a strain of mice expressing high levels of LDL receptors was established.

Their work laid the groundwork for drugs called statins that block cholesterol synthesis, increase LDL receptors, lower blood cholesterol and prevent heart attacks.

LDL receptors on the liver play an important role in removing LDL from circulation.

Without human growth hormone the liver cells cease to function properly which reduces the amount of LDL receptors in the liver itself.

Also remenber that not all people are the same, as some are more resilient to disease than others and some persons have lower / highter LDL receptors than others, that may being forth the risk of atherosclerosis and plague formation.

And he said that what you're really trying to do is you're trying to upregulate the expression of what are called the LDL receptors, right, so you're able to clear cholesterol from the bloodstream more quickly.

A diet high in saturated fat and cholesterol decreases the number of LDL receptors, which reduces the feedback mechanism that tells the liver that no more cholesterol is necessary and therefore leads to higher cholesterol levels.

As you age, the LDL receptors are damaged, but this damage is accelerated in various diseases, such as diabetes.

According to Cordain, saturated fats cause downregulation of the LDL receptors and via that mechanism can promote heart disease.

Insoluble fiber causes digestive problems for many people and saturated fat down regulates LDL receptors.

Furthermore, positive associations between TSH and LDL as well as total cholesterol levels have been found in cross-sectional studies in euthyroid healthy subjects, and the strength of these associations seems to depend on an individual's insulin sensitivity.We therefore hypothesize that the KD has diminished the production of T3 from T4, thereby reducing the number of LDL receptors and thus reducing LDL particle clearance which might be further impaired due to the missing stimulating effect of insulin on LDL uptake into cells.

1) A genetic Condition called Familial Hypercholesterolemia which affects 1 in 500 people, where a person's liver expresses much less LDL receptors and is therefore unable to clear «used» cholesterol in LDL particles from the blood

It relates to a recently discovered protein PCSK9 and tells a story of how age - related loss of LDL receptors leads to increase in LDL, associated uncontrollable cardiovascular inflammation, and atherosclerotic cardiovascular disease — the main killer -LSB-...]

This gives rise to a distinct, small LDL particle that is cleared less avidly by LDL receptors.

Suppose LDL receptors are so thoroughly suppressed by low T3 that the lipid transport function of LDL is abolished.

Not exact matches

Their experiments in pre-clinical models proved to be successful, confirming lower tumour development with the regulation of the proteins that affect production of VLDL (precursors of LDL) and uptake of LDL by receptors from the liver.

It appears that they can also alter cell function: a specific rice microRNA was shown to bind to and inhibit the activity of receptors controlling the removal of LDL — «bad» cholesterol — from the bloodstream.

This latter observation adds to the expanding body of evidence indicating that brain microvascular endothelial cells lack receptors for chemically modified LDL (27, 28).

↵ 3 The abbreviations used are: HUVEC, human umbilical vein endothelial cell; DiI - Ac - LDL, 1,1 ′ - dioctadecyl - 3,3,3 ′, 3 ′ - tetramethyl - indocarbocyanine acetylated low - density lipoprotein; FACS, fluorescence - activated cell sorting; FGFR, fibroblast growth factor receptor; Flk, fetal liver kinase; ICAM, intercellular adhesion molecule; mAb, monoclonal antibody; PE, phycoerythrin; TNF, tumor necrosis factor; VCAM, vascular cell adhesion molecule.

When an LDL particle (carrying cholesterol) binds to the LDLR, the particle is trafficked into the hepatocyte, and PCSK9 targets the receptor for lysosomal degradation.

Pro12Ala polymorphism in the peroxisome proliferator - activated receptor - γ2 (PPARγ2) is associated with higher levels of total cholesterol and LDL - cholesterol in male caucasian type 2 diabetes patients

Dr. Brown and his colleague, Dr. Joseph L. Goldstein, discovered the low density lipoprotein (LDL) receptor, which controls cholesterol in blood and in cells.