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At least 19 recordsLinked to original sources
PubMed1979

Increase of serum high density lipoprotein with progression and regression of aortic lipid deposition in rats.

The progression and regression of aortic lipid deposition was studied in male ExHC rats. Rats in the progression group were fed an atherogenic diet containing 2% cholesterol, 0.4% sodium cholate and 10% olive oil for periods up to 32 weeks. Rats in the regression group were first fed the atherogenic diet for 16 weeks, and then maintained on a basal low cholesterol diet. Half the rats were killed at 4 weeks and the other half at 16 weeks after cessation of the atherogenic diet. Rat aortas of the progression group contained progressively more lipid pari passu with the duration of cholesterol feeding, but connective-tissue proliferation was absent. Deposited lipid in the aorta of cholesterol-fed rats disappeared very slowly after the rats were returned to the basal diet. serum HDL decreased in the hypercholesterolemic ExHC rats fed the atherogenic diet for 4 weeks. By contrast, serum HDL and apo A-I increased in both hypercholesterolemic ExHC rats fed the atherogenic diet for 32 weeks and slightly hypercholesterolemic ExHC rats fed the basal diet for 16 weeks in the regression period.

Animals↗
PubMed2026

Integrated miRNA-mRNA profiling reveals candidate regulatory relationships associated with high-fat diet-induced muscle lipid deposition in black seabream (Acanthopagrus schlegelii).

High-fat diets are increasingly used in aquaculture due to their protein-sparing effects; however, the post-transcriptional regulatory mechanisms of fish muscle in response to high-fat diets (HFD) remain unclear. In this study, juvenile black seabream were fed either a normal-fat diet (NFD) or a HFD to investigate the miRNA-mRNA regulatory network associated with diet-induced muscle lipid deposition. Oil Red O staining and biochemical analysis showed that high-fat diet feeding markedly increased lipid droplet accumulation and crude lipid content in muscle, indicating significant induction of muscle lipid deposition. Integrated mRNA and miRNA expression profiling revealed substantial transcriptomic and post-transcriptional responses to high-fat diet challenge. A total of 271 differentially expressed genes were identified, including 120 upregulated and 151 downregulated genes. Through combined target prediction and expression correlation analysis, thirteen candidate inverse miRNA-mRNA relationships were subsequently identified, and RT-qPCR supported the expression patterns of selected miRNAs and mRNAs. These pairs included miR-499-x-dmgdh, miR-499-y-gatm, miR-727-y-ass1, miR-4649-x-foxo4, miR-9129-z-myl7, and several novel miRNA-mediated interactions involving adk, chst11, lypla2, frem2, kcnc4, wars1, bag2, and capn2. Functional analysis suggested that these regulatory pairs were mainly associated with metabolic adaptation, structural remodeling, and cellular stress responses. In particular, gatm, dmgdh, ass1, and adk were associated with energy metabolism-related processes, including pathways previously linked to Ampk regulation, whereas myl7, frem2, and kcnc4 may contribute to muscle structural maintenance and excitability regulation. Overall, this study provides candidate miRNA-mRNA regulatory relationships potentially involved in high-fat diet-induced muscle lipid deposition and adaptive remodeling in black seabream, offering a basis for future functional studies on muscle metabolism and quality regulation in marine fish.

Animals↗
PubMed1978

Fatty acid accumulation and abnormal lipid deposition in peripheral and border zones of experimental myocardial infarcts.

Twenty-eight dogs with acute anterior myocardial infarcts due to proximal occlusion of the left anterior descending coronary artery (LAD) were studied at various periods following the occlusion to determine: (a) the time course and location of abnormal lipid accumulation after infarction, (b) the degree of muscle-cell injury associated with increased lipid deposition, and (c) whether uptake of fatty acid from the circulating fat pool contributes to lipid accumulation in certain myocardial regions. The findings show that myocardial lipid accumulation begins as early as 6 hr after proximal LAD occulsion. The increased lipid deposition occurs as nonmembrane-bound lipid droplets in muscle cells with and without ultrastructural evidence of irreversible injury. Analysis of tissue uptake of intravenoulsy injected [14C] oleic acid conjugated with albumin revealed relatively selective concentration of label in the peripheral and border regions of the infarct, but occasionally even the central subendocardial portion of the infarct concentrated the fatty acid. Thin-layer chromotography showed that most of the label was associated with the triglyceride fraction when the radiolabeled fatty acid was injected 6 or 24 hr after LAD occlusion. These myocardial cellular and topographical alterations will have to be considered when labeled fatty acids are used for imaging acute myocardial infarcts and/or if attempts are made to identify myocardial fat-laden cells scintigraphically.

Animals↗
PubMed1979

Reduction of hepatic lipid deposition in laying hens by dietary selenium-yeast interaction.

Experiments were conducted to study the effect of chromiun and selenium on liver lipid deposition and incidence of liver hemorrhage in caged layers. Commercial strains of layers were fed ad libitum equicaloric and isonitrogenous diets. Corn-torula dried yeast diets containing added selenium (.1 microgram/g) with or without supplementary chromium (10 microgram/g) significantly reduced total liver lipid and liver hemorrhage. The effects of protein source (soybean meal vs. yeast) and selenium were separated in a factorial experiment which showed that the hepatic lipid response to selenium results from an interaction of selenium with an unidentified factor in torula yeast. The addition of selenium to diets with each protein source significantly elevated glutathione peroxidase (GSHPx) activity. Inclusion of 5% brewers yeast in the corn-soy diet or vitamin E (50 IU/kg) to the corn-torula dried yeast reduced liver lipid similar to that seen in birds fed the torula-yeast diet containing .1 microgram Se/g. Comparison of oral glucose tolerance of birds fed corn-soy and corn-soy brewers yeast diets showed no significant difference. None of the dietary treatments significantly altered body weight, egg production, egg weight, or feed consumption. The results indicate that the metabolic role of selenium in relation to its role in hepatic lipid metabolism is mediated through an interaction with a dietary factor(s) present in yeast.

Animal Feed↗
PubMed2026

Dietary naringenin modulates antioxidant status and hepatic lipid deposition in marine medaka (Oryzias dancena) fed a high-fat diet.

High-fat diets (HFDs) are widely used in aquaculture to improve growth and feed efficiency; however, prolonged feeding can disrupt lipid metabolism, induce oxidative stress, and impair physiological homeostasis. This study evaluated the protective effects of dietary naringenin against HFD-induced physiological alterations in the marine medaka Oryzias dancena. Fish were randomly assigned to one of four dietary treatments and fed the respective experimental diets for 45 days: a normal-fat diet (NFD, 8% crude lipid), a high-fat diet (HFD, 15% crude lipid), or an HFD supplemented with either 0.075% or 0.15% naringenin. Compared with the NFD group, HFD feeding impaired antioxidant status, altered the expression of genes associated with antioxidant defence and lipid metabolism, and promoted hepatic lipid accumulation. Dietary naringenin, particularly at 0.15%, mitigated these adverse effects by restoring muscle superoxide dismutase activity, enhancing total antioxidant capacity, reducing lipid peroxidation, partially normalizing the expression of lipid metabolism-related genes, and alleviating hepatic lipid vacuolation. These findings indicate that dietary naringenin improves antioxidant defence and helps maintain lipid metabolic homeostasis under high-fat feeding conditions, highlighting its potential as a functional dietary additive for aquaculture.

Animals↗
PubMed1979

Cellular pathology of homozygous familial hypercholesterolemia.

Tissues were studied from four subjects with homozygous familial hypercholesterolemia (FH). The specimens consisted of tissues obtained from a 20-week-old fetus at autopsy, samples from a 9-year-old girl during open-heart surgery, and biopsies of cutaneous xanthomas from a 13-year-old girl and a 21-year-old man. The FH fetus, but not the 3 control fetuses, exhibited multifocal lipid deposition particularly involving the stromal cells of the thymus, spleen, and skin and both the stromal and parenchymal cells of the kidney. Only one minute focus of intimal lipid accumulation was found in the aorta and coronary arteries of the FH fetus. A segment of the ascending aorta from the 9-year-old girl showed: 1) foam-cell transformation of many medial smooth-muscle cells, 2) abnormal vascularization of the inner media and intima, and 3) intimal involvement by a typical artherosclerotic plaque with lipid deposits in thin, elongated cells that showed some myocytic features and in foam cells that lacked such features. The mitral and aortic valves of this patient also contained numerous foam cells and showed mild to moderate fibrous thickening. A segment of the saphenous vein, however, contained no lipid deposits. The three xanthomas from two FH homozygotes exhibited marked lipid accumulation in histiocytic foam cells but no lipid deposits in the endothelium of blood vessels in the lesions. The findings in this study, in conjunction with those reported in studies of other FH homozygotes, indicate that homozygous FH is characterized by accelerated atherosclerosis and prominent lipid accumulation in macrophages and other stromal cells of the aortic and mitral valves, skin, tendon, and, varibly, in other extravascular sites. Since most of the intracellular lipid was in the form of non-membrane-bound neutral lipid droplets, it appears that the cytoplasm is the major site of lipid storage in this disease.

Adolescent↗
PubMed1977

Lipid keratopathy following corneal hydrops.

A case of lipid keratopathy occurred following acute rupture of Descemet membrane. The cause of the hydrops remained undetermined. There was no history of any prior corneal inflammation or vascularization in the initially involved eye. Lipid deposition was observed following resolution of the corneal edema, and its course was followed for the next several months. Histopathologic studies of the specimen showed lipid deposits in the posterior and middle corneal stroma and degenerative changes in the corneal lamellae and Bruch membrane. Laboratory examination disclosed a type IV hyperlipemia, with normal serum cholesterol levels and elevation of pre-beta-lipoproteins and triglycerides. It cannot be determined from our study if this condition was a causative factor.

Adult↗
PubMed1979

Nutrition imbalance and angiotoxins as dietary risk factors in coronary heart disease.

Imbalancing nutritionally adequate diets with an excessive amount of fat calories and cholesterol has obscured the fact that intimal thickening occurs spontaneously in time on low-fat cholesterol-free diets during the aging process, and that intimal thickening can be accelerated by dietary angiotoxic "risk factors." Electron microscopy of arterial tissue from animal models identified degenerated smooth muscle cells in the fetus from sows kept on low-fat cholesterol-free diets. After birth, the degenerated smooth muscle cells increased in number with age. The presence of angiotoxic "risk factors" such as oxidized cholesterol and vitamin D3 (cholecalciferol) in the diet of such animal models increased the frequency of smooth muscle cell death in their arteries. Two types of pathology could be developed in the thoracic aorta by continuous or short term feeding of 12.5 times more vitamin D than normally present in commercial rations: 1) a diffuse fibroelastic intimal thickening in the thoracic aorta (arteriosclerosis) with no evidence of lipid deposition by continuous feeding of vitamin D or 2) an initimal thickening in the thoracic aorta and intimal thickening with foam cells and extracellular lipid deposits (atherosclerosis) in the coronary arteries after a short period of supplemental vitamin D followed by 3 to 4 months of supplement-free diets. These two types of arterial damage were identical to that in the plugs of thoracic aorta obtained as a by-product of elective coronary bypass surgery. Although all of the possible sources of oxidized cholesterol in the diet have as yet not been identified, laboratory studies have identified oxidized cholesterol as an angiotoxic factor. Since population groups that consume less vitamin D-supplemented foods, less deep fat fried cholesterol-containing foods, and less hydrogenated fats have a lower incidence of coronary heart disease than Americans, it seems judicious for food processors to reduce these previously unconsidered risk factors to a minimum. This could be done by eliminating vitamin D2 and D3 from all vitamin supplements, from all food and cereal products and from the diet of livestock 1 month before they were killed so that the intake of vitamin D is no larger than the 400 IU/quart in milk which is necessary to prevent rickets in children. Deep fat fryers, which are kept at almost 200 C for 24 hr/day, could perhaps be replaced with microwave ovens in fast food chain outlets. Processors could hydrogenate vegetable oils to a minimum trans fatty acid content and rearrange this fat with polyunsaturated fats to produce high polyunsaturated fats trans-free margarines and shortenings.

Aging↗
PubMed1979

Fabry's disease. Primary diagnosis by electron microscopy.

Fabry's disease is a lipid storage disease found in children and adults. The lipid is stored as a myelin-figure-like whorl of membranes in endothelial and smooth muscle cells, myocardium, fibroblasts, and epithelial cells of the glomerulus. The lipid deposits are identifiable by light microscopy, but are much easier to demonstrate by electron microscopy. The disease leads to vascular insufficiency because of narrowing and thrombosis of arteries and arterioles. The resultant vascular insufficiency leads to peripheral neuritis, myocardial infarction, peripheral infarction and cerebral infarction. Corneal clouding due to lipid deposits is also seen. Renal involvement is widespread, but renal failure occurs late.

Adult↗
PubMed2025

Growth Hormone Alleviates Atherosclerosis Through Regulating the Activity of PI3K/AKT Pathway: Insights From Single-Cell Sequence and Mechanism Exploration.

PURPOSE: This research sought to investigate the impact and underlying mechanisms of growth hormone (GH) on atherosclerosis (AS) based on the analysis of single-cell RNA sequencing (scRNA-seq) data. METHODS: We analyzed the impact of GH on arterial vascular smooth muscle cells (VSMCs) by utilizing scRNA-seq data obtained from both atherosclerotic and healthy vascular tissues in mice. AS was induced in C57BL/6 and ApoE-/- mice through hypophysectomy performed via the parapharyngeal approach, followed by a high-fat diet (HFD), resulting in the C57-Hx and ApoE-/--Hx models. AS was evaluated by measuring arterial lipid deposition, plaque progression, collagen loss, vascular inflammation, and oxidative stress. Serum metabolite alterations were assessed using liquid chromatography-mass spectrometry (LC-MS). RNA sequencing was employed to examine the underlying mechanisms of GH in the context of AS treatment, with findings further confirmed through western blot analysis. In vitro experiments involved treating VSMCs with oxidized low-density lipoprotein (ox-LDL) to simulate atherosclerotic injury. The formation of foam cells was evaluated by measuring lipid accumulation, inflammatory responses, apoptosis, and the expression levels of foam cell-related markers. Finally, the PI3K/AKT inhibitor LY294002 confirmed that GH alleviates AS via the PI3K/AKT signaling pathway. RESULTS: scRNA-seq data analysis showed that growth hormone signaling was reduced in VSMCs of atherosclerotic arteries. HFD led to elevated levels of serum total cholesterol (TC), triglycerides (TGs), and low-density lipoprotein cholesterol (LDL-C), accompanied by increased lipid deposition, inflammatory responses, and oxidative stress. In contrast, high-density lipoprotein cholesterol (HDL-C) and insulin-like growth factor 1 (IGF-1) levels were lower in C57-Hx mice. GH treatment improved HFD-induced AS in ApoE-/--Hx mice. LC-MS analysis revealed that GH altered lipid metabolism in serum samples from C57-sham, C57-Hx, ApoE-/--Hx, and ApoE-/--Hx-GH(3) mice. GH maintained lipid balance by increasing 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (POPC), PE-NMe2(18:1(9z)/18:1(9z)) (DMPE), and 4-chloro-2-nitrobenzylalcohol levels and decreasing 1-heptadecanoyl-sn-glycerol-3-phosphocholine. RNA sequencing showed significant gene expression differences in the aortas of C57-sham and C57-Hx mice. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that GH inhibited the progression of AS by modulating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, a finding that was validated through western blotting. Further in vitro studies demonstrated that GH exerted protective effects on VSMCs against ox-LDL-induced damage through activation of the PI3K/AKT pathway, as evidenced by experiments using the specific PI3K inhibitor LY294002. CONCLUSION: GH alleviates the development of AS through the activation of the PI3K/AKT pathway. The findings of this research emphasize the therapeutic potential of GH in inhibiting AS and highlight the importance of the PI3K/AKT pathway as a promising target for clinical intervention.

PI3K/AKT signaling pathway↗
PubMed1975

Effect of sex and season on the production and deposition of lipid and glycid reserves in the intermittently starving golden hamster.

In golden hamster adapted to intermittent starvation (with access to food for 3 days a week only), the glycogen and lipid content of the liver, total body fat and RQ values measured in vivo were investigated. These parameters were studied in dependence on the duration of the adaptation period (6 weeks versus 20 weeks), season of the year (winter versus summer) and sex. The liver glycogen content in intermittently starved males and females increases after 6 weeks of adaptation during winter. In summer an increase was found after long-term adaptation, but only in males. Male hamsters also exhibited a higher ability to accumulate liver lipids during both seasons. In spite of their lower weight intermittently starving males have a higher percentage of body fat in comparison with females, a stimulating effect being observed in winter. Increased lipogenesis in golden hamsters adapted to intermittent starvation may be concluded from the increased RQ values when compared with relative data gained in controls fed daily ad libitum. Significant differences between RQ measurements according to season and sex were not found.

Adaptation, Physiological↗
PubMed1979

Lipid structure and the behavior of cholesteryl esters in monolayer and bulk phases.

The behavior of cholesteryl esters at the air-buffer interface was studied as a function of molecular area and the presence of noncholesterol-containing lipids (colipids). The data obtained indicate that cholesteryl esters with other than long, saturated acyl groups can be present in surface phases up to packing densities approximately those in natural membranes. Their apparent molecular areas in such phases, which are largely determined by colipid structure, suggest their orientation with the ester function toward the interface. The extent of miscibility in the surface phase is also a strong function of colipid structure. Reversibility of the monolayer to bulk phase transition is determined exclusively by the acyl structure of the cholesteryl ester. Of the esters examined, only those with cis unsaturation collapsed reversibly. Our data predict that cholesteryl esters should be present in small, but finite amounts on the surface of arterial lipid deposits and that a prerequisite for the removal of such deposits is that the bulk lipid phase be in a liquid or liquid crystalline state.

Chemical Phenomena↗
PubMed1977

Bilateral central lipid infiltrates of the cornea.

A 55-year-old woman developed a skin rash and lipid deposition centrally in previously normal corneas. Despite a family history of coronary artery disease, no serum lipid abnormality was detected. Lipid droplets and granules were deposited throughout the corneal epithelium and stroma. Histochemical stains were positive only for phosopholipid and galactolipid. After a keratoplasty, deposition of similar lipid material recurred in the graft. An inflammatory process and increased corneosceleral limbal vascular permeability may have accounted for the unusual corneal findings in this patient.

Cerebrosides↗
PubMed1976

The retina in type 5 hyperlipoproteinemia.

Of two patients with type 5 hyperlipoproteinemia, one exhibited lipemia retinalis with multiple retinal hemorrhages and intraretinal lipid extravasations. Postmortem examination showed hemorrhages in the inner retinal layers and lipid deposits largely in the outer plexiform layer. Lipid within the walls of the retinal vessels was demonstrated by light and electron microscopy. The second patient exhibited visual loss due to progressive obstruction of retinal vessels with white material presumed to be lipid. Findings were confined to one eye.

Adult↗