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Results for “Lipid Droplets”

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At least 19 recordsLinked to original sources
PubMed1975

Analyses of renal medullary lipid droplets from normal, hydronephrotic, and indomethacin treated rabbits.

Lipid droplets isolated from rabbit renal medullary tissue were analyzed and found to be composed of triglyceride and free fatty acids in a ratio of 2.9:1. These triglycerides were unique when compared to triglycerides of other rabbit tissues examined, in that they contained high percentages of octadecanoic acid (stearic acid, 9.8%), 5,8,11,14-eicosatetraenoic acid (arachidonic acid, 6.8%), and 7,10,13,16-docosatetraenoic acid (adrenic acid, 10%). Lipid droplet triglycerides were found to increase during experimental hydronephrosis and after administration of indomethacin, a prostaglandin synthetase and phosphodiesterase inhibitor. From gas liquid chromatography of fatty acid methyl esters of these triglycerides, it was determined that they were enriched further in their percent composition of 9,12-octadecadienoic acid (linoleic acid) and arachidonic acid, a prostaglandin precursor. The inverse relationship between lipid droplets and prostaglandin content in the inner medulla suggested a significant role of lipid droplet triglycerides as storage pools for prostaglandin precursors.

Animals↗
PubMed1992

Effect of chronic ACTH treatment on the physical state of lipid droplets in rat adrenocortical cells.

A histophysical method has been adapted to determine the thermotropic phase transitions of adrenocortical lipid droplets using a polarizing microscope equipped with a cold/hot stage. Cryosections of freshly-removed, unfixed adrenals, derived from control (untreated), and 14 days ACTH-treated rats were examined. The lipid droplets in the zona fasciculata and zona reticularis of the untreated rats were birefringent at room temperature (22 degrees C). The birefringence of zona glomerulosa lipids selectively increased in the temperature range from -10 to -15 degrees C. In cryosections prepared from ACTH-treated rats, thermotropic phase transitions of the lipid droplets appeared at a temperature range between -30 and -40 degrees C in each cortical zone. The chemical analysis of the isolated lipids revealed that the relative amount of triglycerides in the zona fasciculata lipids increased, while that of free and esterified cholesterol decreased after chronic ACTH treatment. Present data suggest that the increased fluidity of lipid droplets promotes lipid mobilization in response to the enhanced demand of the chronically stimulated adrenocortical cells. Viscosity-dependent mobilization of free cholesterol from lipid droplets is not a rate-limiting process in adrenal steroidogenesis, but rather may represent an important control of the availability of precursor from lipid stores.

Adrenal Cortex↗
PubMed1977

Lipid droplet of sebaceous carcinoma. Electron microscopic study utilizing glycol methacrylate-glutaraldehyde-urea procedure.

The ultrastructure of lipid droplets of sebaceous carcinoma (Meibomian gland carcinoma) was studied by conventional methods and a lipid-retention procedure. Two different structures were clearly differentiated by the latter technique. The peripheral part of the lipid droplet was composed of whirled lamellar structures (myelin-like structures) while the interior appeared to be continuously homogenous. The lamellar structures were presumed to have come from smooth-surfaced endoplasmic reticulum, and to transform to the amorphous material-triglyceride-during maturation of the lipid droplets. A true limiting membrane or membranous shell around the lipid droplet was not deceted.

Aged↗
PubMed2025

The Myo2 adaptor Ldm1 and its receptor Ldo16 mediate actin-dependent lipid droplet motility.

Organelle motility enables strategic cellular reorganizations. In yeast, this process depends on the actin cytoskeleton, type V myosin motor proteins, and organelle-specific myosin adaptor proteins. While the myosin adaptors for most organelles are known, the coupling of myosin to lipid droplets (LDs), the cellular lipid storage organelles, remained enigmatic. Using genome-wide screening, we identified Ldm1 (lipid droplet motility 1/Yer085c) as a myosin adaptor. Ldm1 binds to the globular tail domain of the myosin Myo2 and to the LD surface protein Ldo16 to enable actin-dependent LD motility. Ldo16 has additional roles in LD contact sites to the vacuole and the endoplasmic reticulum, suggesting a coordination of LD motility and organelle tethering. Ldm1 has a second role in mitochondrial transport, and elevated Ldm1 levels rescue defects of the mitochondrial Myo2-adaptors Mmr1/Ypt11. Our work identifies the molecular machinery for LD motility and contributes to a comprehensive understanding of acto-myosin-based cellular reorganization.

Lipid Droplets↗
PubMed1975

Acute effects of ACTH on dissociated adrenocortical cells: quantitative changes in mitochondria and lipid droplets.

To study the role of certain organelles in steroidogenesis, dissociated rat adrenocortical cells were incubated for two hours with ACTH at a concentration that induces a high level of steroid production. Sections of ACTH treated and untreated cells were photographed in the electron microscope, and morphometric analysis was undertaken to assess possible ACTH-induced changes in total cell volume, volume density and numerical denisty of lipid droplets and mitochondria. There was no change in total cell volume. Lipid droplet volume density and numerical density decreased. Mitochondrial volume density did not change, but numerical density increased. The decrease in lipid droplet volume density indicates a rapid depletion of cholesterol for steroid production. This depletion is almost entirely due to the disappearance of lipid droplets, rather than to an overall diminution in their size, as shown by the decrease in lipid droplet numerical density. The mitochondrial data suggest that the adrenocortical cell has an adedquate mitochondrial apparatus to respond to acute ACTH stimulation with increased steroid output without an increase inmitochondrial volume.

Adrenal Cortex↗
PubMed1992

A mixture of paraphenylenediamine and imidazole: its effect on the extraction of lipid droplets during electron microscopy staining.

To prevent extraction of lipids during a double staining procedure for electron microscopy, the tissue slices, double fixed with glutaraldehyde and osmium tetroxide to preserve microvesicular lipid droplets in the cytoplasm, were immersed for 2 hr in veronal buffer (pH 9.0) containing 0.5% p-phenylenediamine and 0.5% imidazole immediately after postfixation. The stained sections of the immersed tissue slice showed blackened, well circumscribed lipid droplets similar to those in corresponding unstained sections. Moreover, highly contrasting features of the cellular architecture could be visualized with the double stained, as well as routinely prepared sections.

Adrenal Cortex↗
PubMed1979

Studies on intrarenal prostaglandins. Effect of unilateral renal artery constriction on lipid droplets in the medullary interstitial cells of the 'opposite' kidney in rabbits.

The unilateral renal artery in rabbits was constricted, and lipid droplet count in the medullary interstitial cells of the 'opposite' kidney was performed 1 week after surgery. Lipid droplet count in hypertensive rabbits was less than that in both nonhypertensive and normal rabbits and was inversely proportional to the mean blood pressure. Lipid droplet count was significantly correlated with the juxtaglomerular granulation index and the sodium content in the inner medulla. The present results suggest that, in the opposite kidney of rabbits hypertensive due to unilateral constriction of the renal artery, the enhanced release of prostaglandins and the washout of solute in the renal medulla may be induced as a response to increased perfusion pressure and elevated circulating angiotensin.

Animals↗
PubMed1975

Lipid droplet accumulation in cardiac muscle cells of the bat: potential auto-toxicity of the cardiac sympathetic innervation.

The previously described ability of reserpine and parachlorophenylalanine to induce the accumulation of lipid droplets in ventricular cardiac muscle cells of the bat was investigated. Lipid droplet accumulation was assessed qualitatively by light microscopy and quantitatively by morphometric analysis of electron micrographs. An hypothesis that the action of the drugs was an indirect one, mediated by the cardiac adrenergic innervation, was framed and tested. Lipid droplet accumulation occurred during a time of intense sympathetic activity, that of arousal from hibernation. The ability of the two drugs to produce the effect was antagonized by prior sympathetectomy with 6-hydroxy-dopamine. The effect was mimicked by administration of exogenous norepinephrine together with inhibitors of its catabolic enzymes, monoamine oxidase and catechol-o-methyl transferase. These observations are all consistent with the initial hypothesis and raise the possibility that endogenous norepinephrine in the cardiac sympathetic innervation might be, at least potentially, auto-toxic.

Animals↗
PubMed2026

A Phosphoproteomic Platform Identifies Erythrocyte Membrane Protein Band 4.1-Like 3-Mediated Lipid Droplet Remodeling Linked to Liver Cancer Invasion and Migration.

Aberrant lipid metabolism is a hallmark of hepatocellular carcinoma (HCC), yet the regulatory mechanisms governing lipid droplet (LD) dynamics and their contribution to tumor progression remain poorly understood. Here, we developed an ultrasensitive phosphoproteomic platform using high-affinity HPDA@Ti4+ nanospheres to map LD-associated phosphorylation events across six HCC cell lines. By correlating phosphoproteomic signatures with LD morphology, we identified distinct regulatory signatures associated with LD size and abundance. Functional perturbation screens identified two distinct phosphoprotein modules controlling LD size: silencing SH3KBP1, SLK, EHD2, EPB41L3, and NEXN reduced LD size in Huh1 cells, whereas silencing CPD, BET1, UFL1, RRP1B, OGFR, and CD2BP2 enlarged LDs in Huh7 cells. Notably, we identified EPB41L3 as a critical metabolic-metastatic link; its loss decreased LD size and accelerated HCC migration and invasion, correlating with poor clinical prognosis. Crucially, we identified five key phosphorylation sites on EPB41L3 essential for its function; substituting these with alanine completely abolished its regulatory control over both LD size and HCC metastatic potential. Together, these findings delineate a phosphorylation-based regulatory network controlling the LD architecture and metastatic potential in HCC. Our study not only identifies potential therapeutic targets but also establishes a generalizable phosphoproteomic framework for interrogating lipid signaling in cancer metabolism.

Humans↗
PubMed1979

Postnatal changes in the distribution of lipid droplets within the liver lobule of the mouse.

The changes in the distribution of lipid droplets in the liver lobule were studied during the postnatal development of the mouse. At birth, and 1 day after birth, lipid droplets were evenly distributed throughout the lobule. A slightly uneven distribution of the droplets, more in centrilobular areas, appeared 2 days after birth. After this the difference in the number of droplets between the cells of the centrilobular and periportal areas became progressively more marked reaching a maximum by 17 days of age, and then decreasing to the adult level between 21 and 24 days. Thus, heterogeneity among hepatocytes with respect to lipid content is not present in newborn mice but develops gradually during the postnatal development.

Aging↗
PubMed2025

Hepatocyte-specific CLSTN3B ablation impairs lipid droplet maturation and alleviates diet-induced steatohepatitis in mice.

Excessive lipid accumulation in hepatocytes, a hallmark of metabolic dysfunction-associated steatotic liver disease (MASLD), can lead to progressive liver damage. Understanding the molecular mechanisms governing lipid storage in hepatocytes is essential for identifying therapeutic targets to halt MASLD progression. Here, we show a pivotal role for the protein calsyntenin 3β (CLSTN3B) in promoting lipid droplet (LD) maturation and lipid storage in hepatocytes. Previously characterized as an endoplasmic reticulum (ER)-LD contact protein that facilitates LD maturation in adipocytes, we now show that CLSTN3B expression is strongly induced in mouse hepatocytes by peroxisome proliferator-activated receptor gamma (PPARγ) in response to dietary caloric excess. Hepatocyte-specific deletion of CLSTN3B in mice significantly increases energy expenditure, reduces metabolic efficiency, and protects against diet-induced hepatic steatosis and fibrosis. Mechanistically, CLSTN3B deficiency causes reduced LD phospholipid coverage and increased lipase recruitment. This results in enhanced fatty acid oxidation driven by a futile cycle of lipolysis and re-esterification. Notably, human clinical data reveal a positive correlation between hepatic CLSTN3B expression and MASLD severity and progression, emphasizing its relevance to human disease. Together, our findings establish CLSTN3B as a key regulator of hepatocyte lipid storage and metabolic efficiency and highlight its potential as a therapeutic target in MASLD.

Journal Article↗
PubMed1979

The occurrence of lipid droplets in the proximal and distal tubules of the rat kidney after folic acid treatment.

Folic acid in high doses gives rise to an accumulation of lipid droplets in the kidney in addition to other changes in the epithelial of both proximal and distal tubules. With the administration of methionine a decrease of lipid droplets and an improvement of the structures of most of the membranes and mitochrondria are observed. These findings have been discussed in regard to the theory of the "chemically induced hyperplasia of the kidneys" related to folic acid.

Animals↗
PubMed2026

Comparative lipidomics of iPSC-derived microglia protocols reveal lipid droplet and immune differences mediated by media composition.

Altered microglial lipid metabolism is heavily implicated in Alzheimer's disease (AD) and aging. Recently, protocols were developed to generate human induced pluripotent stem cell-derived microglia-like cells (iMGL) to study microglial function in vitro, including embryoid body-based methods and induced transcription factor (iTF)-dependent approaches. Here, we performed comparative lipidomics on iMGL from these methods and report major differences in multiple lipid classes, including triglycerides (TGs), a storage form of fatty acids implicated in microglial reactivity. TGs are strongly increased in iTF microglia due to the absence of a media supplement (B-27). Supplementing iTF microglia with B-27, or its component L-carnitine, reduces TGs and promotes a homeostatic state. B-27 also renders iTF microglia metabolically responsive to immune stimuli. Overall, our data show that iMGL differentiation methods have a major impact on microglial lipidomes and warrant attention when studying AD and neuroinflammatory processes involving lipids.

Microglia↗
PubMed1977

An electron microscopic study of sebaceous epithelioma. A case report with two new observations on lipid droplet formation.

A lesion presenting a typical histopathological picture of sebaceous epithelioma comprised three kinds of cells; immature, transitional, and mature cells corresponding to the components of the normal sebaceous gland. Melanocytes and melanosomes were absent. These findings clearly distinguished the tumor from basal cell epithelioma, and it was concluded that sebaceous epithelioma represents a primary neoplasm of the sebaceous gland. New observations on lipid droplet formation are made with regard to the glycogen-containing cytolysome - tentatively designated a Liposome - and membrane structures around the lipid droplet found in mature cells.

Aged↗
PubMed1975

Lipid droplets in the heart interstitium: concentration and distribution.

A morphological study of the sudanophilic lipids in dog and human hearts was carried out. The hearts of 5 mongrel dogs and 20 auricular appendices of human patients were utilized. The dog hearts were fixed in situ by perfusion with 2% glutaraldehyde, and the human tissue was fixed by immersion. For the ultrastructural study, some blocks of every portion of the specimen were postfixed in osmium and embedded in Epon. The topographical and quantitative study was done on frozen 20-mu sections of tissue stained with Sudan IV in propylene glycol and counterstained with hematein (Geigy). The results indicate that a significant quantity of visible triglycerides is extracellular and located in the interstitial spaces of the heart. The dimensions of these lipid droplets vary from 0.5 mu to more than 20 mu. The highest concentration was found in the epicardial region of the left ventricle, but a significant amount was found in the endocardium and in the middle portion of the myocardium. These observations indicate that a sizable portion of the heart interstitium is occupied by free droplets of triglycerides. This substrate pool is probably mobile and readily available as a source of energy.

Adipose Tissue↗
PubMed1978

Lipid droplets in the lining epithelium of the crop of Columba livia.

Presence and distribution of lipid were studied in the lining epithelia of three regions of the pigeon (Columba liva) crop: lateral lobes, median region near the cervical esophagus and median region near the thoracic esophagus. During the resting phase of the 'milk gland', insulated lipid droplets were observed within the lining epithelium of the three regions studied. On the other hand, during the activity of the 'milk gland' (under action of exogenous prolactin and in natural incubation), only the lateral lobes showed a remarkable increase in the amount of lipid, whereas both median regions showed only an inexpressive increase of lipid within their epithelium.

Animals↗
PubMed2025

Plasma membrane accessible cholesterol is regulated by ACC1 and lipid droplets.

Proper maintenance of plasma membrane (PM) cholesterol is essential for diverse processes ranging from animal development to pathogen evasion. Despite decades of study, the mechanisms governing cellular cholesterol regulation are incomplete. Using genome-wide screens we find that ACC1, the rate-limiting enzyme in fatty acid biosynthesis, regulates PM cholesterol transport. ACC1 loss causes a ~10-fold increase in PM accessible cholesterol in cells and mice. Mechanistically, we find that ACC1 regulates lipid droplet (LD) catabolism, and LDs are intimately tied to PM accessible cholesterol levels since reductions or elevations in their numbers block or promote cholesterol trafficking, respectively. Furthermore, LDs are required for cholesterol trafficking induced by 25-hydroxycholesterol, a modulator of inflammation and an interferon-stimulated second messenger that protects cells from pathogen invasion. This work identifies an unrecognized role for ACC1 and LDs in cholesterol regulation, which has implications for diseases where LD numbers are altered, from metabolic syndromes to neurodegeneration.

25-hydroxycholesterol↗