Fat-storing Cells Research Articles

AP-1/C-FOS and AP-1/FRA2 differentially regulate early and late adipogenic differentiation of mesenchymal stem cells.

Obesity is defined as an abnormal accumulation of adipose tissue in the body and is a major global health problem due to increased morbidity and mortality. Adipose tissue is made up of adipocytes, which are fat-storing cells, and the differentiation of these fat cells is known as adipogenesis. Several transcription factors (TFs)such as CEBPβ, CEBPα, PPARγ, GATA, and KLFhave been reported to play a key role in adipogenesis. In this study, we report one more TFAP-1, which is found to be involved in adipogenesis. Human mesenchymal stem cells were differentiated into adipocytes, and the expression pattern of different subunits of AP-1 was examined during adipogenesis. It was observed that C-FOS was predominantly expressed at an early stage (Day 2), whereas FRA2 expression peaked at later stages (Days 6 and 8) of adipogenesis. Chromatin immunoprecipitation-sequencing analysis revealed that C-FOS binds mainly to the promoters of WNT1, miR-30a, and ANAPC7and regulates their expression during mitotic clonal expansion. In contrast, FRA2 binds to the promoters of CIDEA, NOTCH1, ARAF, and MYLK, regulating their expression and lipid metabolism. Data obtained clearly indicatethat the differential expression of C-FOS and FRA2 is crucial for different stages of adipogenesis. This also raises the possibility of considering AP-1 as a therapeutic target for treating obesity and related disorders.

Rat Hepatic Stellate Cell Line CFSC-2G: Genetic Markers and Short Tandem Repeat Profile Useful for Cell Line Authentication.

Hepatic stellate cells (HSCs) are also known as lipocytes, fat-storing cells, perisinusoidal cells, or Ito cells. These liver-specific mesenchymal cells represent about 5% to 8% of all liver cells, playing a key role in maintaining the microenvironment of the hepatic sinusoid. Upon chronic liver injury or in primary culture, these cells become activated and transdifferentiate into a contractile phenotype, i.e., the myofibroblast, capable of producing and secreting large quantities of extracellular matrix compounds. Based on their central role in the initiation and progression of chronic liver diseases, cultured HSCs are valuable in vitro tools to study molecular and cellular aspects of liver diseases. However, the isolation of these cells requires special equipment, trained personnel, and in some cases needs approval from respective authorities. To overcome these limitations, several immortalized HSC lines were established. One of these cell lines is CFSC, which was originally established from cirrhotic rat livers induced by carbon tetrachloride. First introduced in 1991, this cell line and derivatives thereof (i.e., CFSC-2G, CFSC-3H, CFSC-5H, and CFSC-8B) are now used in many laboratories as an established in vitro HSC model. We here describe molecular features that are suitable for cell authentication. Importantly, chromosome banding and multicolor spectral karyotyping (SKY) analysis demonstrate that the CFSC-2G genome has accumulated extensive chromosome rearrangements and most chromosomes exist in multiple copies producing a pseudo-triploid karyotype. Furthermore, our study documents a defined short tandem repeat (STR) profile including 31 species-specific markers, and a list of genes expressed in CFSC-2G established by bulk mRNA next-generation sequencing (NGS).

Differential cholesterol uptake in liver cells: A role for PCSK9.

The clearance of low-density lipoprotein (LDL) particles from the circulation is regulated by the LDL receptor (LDLR) and proprotein convertase subtilisin/kexin 9 (PCSK9) interaction. Its disruption reduces blood cholesterol levels and delays atherosclerosis progression. Whether other members of the LDLR superfamily are in vivo targets of PCSK9has been poorly explored. The aim of this work was to study the interaction between PCSK9 and members of the LDLR superfamily in the regulation of liver cholesterol homeostasis in an in vivo low-density lipoprotein receptor related protein 5 (LRP5) deficient mice model challenged with high-fat diet. Our results show that Wt and Lrp5-/- mice fed a hypercholesterolemic diet (HC) have increased cholesterol ester accumulation and decreased liver LDLR and LRP5gene and protein expression. Very low-density lipoprotein receptor (VLDLR), LRP6, LRP2, and LRP1 expression levels were analyzed in liver samples and show that they do not participate in Lrp5-/- liver cholesterol uptake. Immunoprecipitation experiments show that LRP5 forms a complex with PCSK9 in liver-specific fat-storing stellate cells but not in structural HepG2 cells. Hepatic stellate cells silenced for LRP5 and/or PCSK9 expression and challenged with lipids show reduced cholesterol ester accumulation, indicating that both proteins are involved in lipid processing in the liver. Our results indicate that cholesterol esters accumulate in livers of Wt mice in a LDLR-family-members dependent manner as VLDLR, LRP2, and LRP6show increased expression in HC mice. However, this increase is lost in livers of Lrp5-/- mice, where scavenger receptors are involved in cholesterol uptake. PCSK9 expression is strongly downregulated in mice livers after HC feeding. However PCSK9 and LRP5 bind in the cytoplasm of fat storing liver cells, indicating that this PCSK9-LRP5 interaction is cell-type specific and that both proteins contribute to lipid uptake.

Electro-physiology Models of Cells with Spherical Geometry with Non-conducting Center

We study the flow of electrical currents in spherical cells with a non-conducting core, so that current flow is restricted to a thin shell below the cell’s membrane. Examples of such cells are fat storing cells (adipocytes). We derive the relation between current and voltage in the passive regime and examine the conditions under which the cell is electro-tonically compact. We compare our results to the well-studied case of electrical current flow in cylinder structures, such as neurons, described by the cable equation. In contrast to the cable, we find that for the sphere geometry (1) the voltage profile across the cell depends critically on the electrode geometry, and (2) the charging and discharging can be much faster than the membrane time constant; however, (3) voltage clamp experiments will incur similar distortion as in the cable case. We discuss the relevance for adipocyte function and experimental electro-physiology.

Histological and histochemical studies of digestive system in the megrim, Lepidorhombus whiffiagonis (Teleostei: Scophthalmidae)

The digestive system of Lepidorhombus whiffiagonis was studied using histological and histochemical techniques. The wall of oesophagus and stomach fundus consisted of four histological layers: mucosa, submucosa, muscularis and the outer layer. Mucosa, the innermost layer, usually consisted of three different layers, including epithelium, lamina propria and lamina muscularis mucosae. Submucosa of connective tissue with blood vessels and nerve fibres underlined the mucosa and usually protrudes into the mucosal folds except in the gallbladder where it is completely absent. The muscular layer of the digestive system consisted of smooth muscles arranged in longitudinal, circular or oblique layers. Striated fibres were found in the oesophageal wall. The outermost layer comes as tunica adventitia in upper parts and tunica serosa in lower parts of the digestive system. Hepatocytes were surrounded by a mass of fat-storing cells. Serous acini of pancreas were scattered down the length of the stomach. Alcian blue/PAS technique revealed that alkaline and neutral mucopolysaccharides were present in oesophagus while acidic mucopoly-saccharides was found in the stomach and intestines.

Thymus aging in mice deficient in either EphB2 or EphB3, two master regulators of thymic epithelium development.

The epithelial microenvironment is involved in thymus aging, but the possible role of EphB receptors that govern the thymic epithelium development has not been investigated. Herein, we study the changes undergone by the thymus of EphB-deficient mice throughout their life. Immune alterations occurring throughout life were more severe in mutant than in wild-type (WT) mice. Mutant thymuses exhibit lower cellularity than WT ones, as well as lower proportions of early thymic progenitors cells and double-positive (CD4+ CD8+ ) thymocytes, but higher of double-negative (CD4- CD8- ) and single-positive (CD4+ CD8- , CD4- CD8+ ) cells. Throughout life, CD4+ naïve cells decreased particularly in mutant mice. In correlation, memory T cells, largely CD8+ cells, increased. Aged thymic epithelium undergoes changes including appearance of big epithelial free areas, decrease of K8+ K5- areas, which, however, contain higher proportions of Ly51+ UEA1- cortical epithelial cells, in correlation with reduced Aire+ medullary epithelial cells. Also, aged thymuses particularly those derived from mutant mice exhibited increased collagen IV, fat-storing cells, and connective cells. The absence of EphB accelerates the alterations undergone throughout life by both thymic epithelium and thymocytes, and the proportions of peripheral naïve and memory T cells, all of which are hallmarks of immune aging.

Making a three-way contact

Cell Biology Membrane contact sites between organelles are important in several cellular functions. Within cells, lipids are stored in specialized organelles known as lipid droplets. In some cell types, lipid droplets interact directly with mitochondria. In adipocytes, which are professional fat-storing cells, Freyre et al. found that the outer mitochondrial membrane protein MIGA2 tethers mitochondria to lipid droplets. They identified a lipid droplet–targeting motif and found that MIGA2 also interacts with the endoplasmic reticulum membrane proteins VAP-A and VAP-B. Depleting MIGA2 severely perturbed adipocyte differentiation. MIGA2 is required for the de novo synthesis of lipids and links mitochondrial lipogenesis and endoplasmic reticulum triglyceride synthesis during lipid-droplet loading. Mol. Cell 10.1016/j.molcel.2019.09.011 (2019).

Zataria Multiflora bois as an auspicious therapeutic approach against Echinococcus granulosus: Current status and future perspectives

Hydatidosis caused by Echinococcus granulosus is a major zoonotic diseases. In addition to imposing heavy economic losses, the disease is a public health problem worldwide. The larval stage of the parasite (hydatid cyst) is formed in a wide range of domestic, wild and human beings as intermediate hosts. On the other, its recurrence has been reported anywhere as a reemerging disease. Although the cysts have some evading mechanisms, both human TH1 and TH2 cells subsets are stimulated. Because of increasing resistance and adverse effects of medications such as abnormalities of liver and other organs functions and abdominal pain, seeking alternative therapeutic approaches to be inexpensive, easy available, with low side effects and toxicity seems essential. However, the lack of information on the social and economic welfares of herbal medicines for the industrial scale application is a limitation. Zataria Multiflora bois (ZMB) has exhibited huge advantages and tremendous protoscolicidal effects as demonstrated by numerous studies and its combination therapies with anti-parasitic drugs have exerted desirable outcomes in vitro and in vivo. Noticeably, the compound confers negligible side effects or toxicity even at high concentrations. ZMB has exhibited promising inhibitory effects against hydatid cyst, particularly when combined with chemical drugs and in formulations of nanoemulsions. Its immunomodulatory effects include increase of nitric oxide production (NO) and protection of hepatic cells (Kupffer cells, fat-storing cells, and endothelial cells), enhancement of macrophages and T cells and increase of cytokines production. This study aimed at assessment of ZMB traits for application against hydatid cyst protoscolices.

Efficacy of Ginger (Zingiber officinale) in Ameliorating Streptozotocin-Induced Diabetic Liver Injury in Rats: Histological and Biochemical Studies.

Ginger (Zingiber officinale) was reported to have an antioxidant, antidiabetic effect. This study was done to investigate its therapeutic effect against functional and structural alteration in liver of diabetic rat (intraperitoneal streptozotocin (STZ) in a dose of 60 mg/kg/bw). Thirty adult male rats (three-months-old and 250 g weight) were sorted into five groups (N=6). G1 used as control, G2 was diabetic rats without any treatment, G3 was diabetic rats given oral ginger in a dose of 500 mg/kg/bw, G4 was diabetic rats treated with metformin (500 mg/kg/bw) while G5 received ginger orally. The experiment lasts for six weeks, animals were anesthetized by ether, body weight was recorded for all animals. Blood was collected for further analysis of lipid profile, liver enzymes and total antioxidant. Liver was dissected, weighted and samples were processed for histopathological study. The results showed significant decrease of glaucous level and liver enzymes in ginger treated rats. Total antioxidant was preserved. Ginger lowered blood glucose, level, regained body weight and liver index to near normal values. Diabetes induced degenerative changes and micro-vesicular lipid deposition in hepatocytes with moderate portal area fibrosis. Ultrastructure study confirmed such changes beside demonstrating increased lipid deposition in fat storing cells. Ginger was found to ameliorate those changes in treated animals. Results were matching metformin effects. In conclusion, Ginger as a natural safe Herbal medication can be used to support liver functions in diabetic status.

Induction of Lymphangiomas by Freund's Incomplete Adjuvant (FIA) in Fatty Acid Binding Protein (FABP)‐3, 5 and 7 Knock‐out Mice

IntroductionIn an FIA‐induced benign lymphangioma model (Mancardi et al., 1999), we have suggested a sequential transformation from peritoneal mesothelial cells to functional lymphatic vessels via fat storing tumor cells after the FIA stimulation (EB2009 & 2015). However, the actual mechanism of the tumorigenesis and cellular involvement have yet to be established. FABPs are known to be involved in the promotion of cellular uptake and transport of fatty acids and the targeting of them to specific metabolic pathways. The aim of this study is, therefore, to investigate the possible involvement of FABPs during the FIA‐induced tumor development using FABP KO mice.Materials & MethodsLymphangiomas were induced in C57BL/6 (B6) mice and FABP3, 5 and 7 KO mice by an intraperitoneal injection of FIA (0.2 ml emulsion). For histological analyses, tissue cryosections were made and immunostained with various antibodies against FABP3, 4, 5, 7, and various lymphatic markers, such as podoplanin (PDPN), LYVE‐1 and LA102.Results & ConclusionsAfter FIA injection, peritoneal mesothelial cells became tall in height losing their polarity and gradually formed stratified cell masses on the peritoneal surface in B6 mice. The tumors became honeycomb‐like lymphangiomas consisted of ring‐like fat storing cells with various sizes. Some fat storing cells fused with each other and gradually formed either tubular structures like lymphatic vessels or huge follicles. These cells were strongly positive for PDPN, F4/80 and FABP5, but negative for FABP4. The follicular structures mainly consisted of FABP7+ cells. Interestingly, only the functional lymphatic vessel‐like structures expressed LYVE‐1 and LA102. In FABP‐KO mice, there was no significant difference in the incidence of tumors as compared with normal B6 mice. However, tumors developed more vigorously in FABP7 KO mice than other KO strains. Among FABP KO mice, relatively smaller fat storing cells were seen in FABP3 KO mice, whereas follicular type structures were more commonly found in FABP5 KO mice. In contrast, the tumors in FABP7 KO mice showed less fat storing cells with more inflammatory and fibrous components. In conclusion, a close relationship between the extrinsic FIA metabolism and the lymphatic system may be suggested in this tumor model, although the actual role and biological significance of each FABP in the tumorigenesis remain to be further clarified.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

CDK6 inhibits white to beige fat transition by suppressing RUNX1

Whereas white adipose tissue depots contribute to the development of metabolic diseases, brown and beige adipose tissue has beneficial metabolic effects. Here we show that CDK6 regulates beige adipocyte formation. We demonstrate that mice lacking the CDK6 protein or its kinase domain (K43M) exhibit significant increases beige cell formation, enhanced energy expenditure, better glucose tolerance, and improved insulin sensitivity, and are more resistant to high-fat diet-induced obesity. Re-expression of CDK6 in Cdk6−/− mature or precursor cells, or ablation of RUNX1 in K43M mature or precursor cells, reverses these phenotypes. Furthermore, RUNX1 positively regulates the expression of Ucp-1 and Pgc1α by binding to proximal promoter regions. Our findings indicate that CDK6 kinase activity negatively regulates the conversion of fat-storing cells into fat-burning cells by suppressing RUNX1, and suggest that CDK6 may be a therapeutic target for the treatment of obesity and related metabolic diseases.

Endoplasmic reticulum oxidase 1α is critical for collagen secretion from and membrane type 1-matrix metalloproteinase levels in hepatic stellate cells

Upon liver injury, excessive deposition of collagen from activated hepatic stellate cells (HSCs) is a leading cause of liver fibrosis. An understanding of the mechanism by which collagen biosynthesis is regulated in HSCs will provide important clues for practical anti-fibrotic therapy. Endoplasmic reticulum oxidase 1α (ERO1α) functions as an oxidative enzyme of protein disulfide isomerase, which forms intramolecular disulfide bonds of membrane and secreted proteins. However, the role of ERO1α in HSCs remains unclear. Here, we show that ERO1α is expressed and mainly localized in the endoplasmic reticulum in human HSCs. When HSCs were transfected with ERO1α siRNA or an ERO1α shRNA-expressing plasmid, expression of ERO1α was completely silenced. Silencing of ERO1α expression in HSCs markedly suppressed their proliferation but did not induce apoptosis, which was accompanied by impaired secretion of collagen type 1. Silencing of ERO1α expression induced impaired disulfide bond formation and inhibited autophagy via activation of the Akt/mammalian target of rapamycin signaling pathway, resulting in intracellular accumulation of collagen type 1 in HSCs. Furthermore, silencing of ERO1α expression also promoted proteasome-dependent degradation of membrane type 1-matrix metalloproteinase (MT1-MMP), which stimulates cell proliferation through cleavage of secreted collagens. The inhibition of HSC proliferation was reversed by treatment with MT1-MMP-cleaved collagen type 1. The results suggest that ERO1α plays a crucial role in HSC proliferation via posttranslational modification of collagen and MT1-MMP and, therefore, may be a suitable therapeutic target for managing liver fibrosis.

The stellate cell system (vitamin A-storing cell system)

Past, present, and future research into hepatic stellate cells (HSCs, also called vitaminA-storing cells, lipocytes, interstitial cells, fat-storing cells, or Ito cells) are summarized and discussed in this review. Kupffer discovered black-stained cells in the liver using the gold chloride method and named them stellate cells (Sternzellen in German) in 1876. Wake rediscovered the cells in 1971 using the same gold chloride method and various modern histological techniques including electron microscopy. Between their discovery and rediscovery, HSCs disappeared from the research history. Their identification, the establishment of cell isolation and culture methods, and the development of cellular and molecular biological techniques promoted HSC research after their rediscovery. In mammals, HSCs exist in the space between liver parenchymal cells (PCs) or hepatocytes and liver sinusoidal endothelial cells (LSECs) of the hepatic lobule, and store 50-80% of all vitaminA in the body as retinyl ester in lipid droplets in the cytoplasm. SCs also exist in extrahepatic organs such as pancreas, lung, and kidney. Hepatic (HSCs) and extrahepatic stellate cells (EHSCs) form the stellate cell (SC) system or SC family; the main storage site of vitaminA in the body is HSCs in the liver. In pathological conditions such as liver fibrosis, HSCs lose vitaminA, and synthesize a large amount of extracellular matrix (ECM) components including collagen, proteoglycan, glycosaminoglycan, and adhesive glycoproteins. The morphology of these cells also changes from the star-shaped HSCs to that of fibroblasts or myofibroblasts.

Effects of Methylmercury exposure in 3T3-L1 Adipocytes

Mercury-containing compounds are environmental pollutants that have become increasingly consequential in the Arctic regions of North America due to processes of climate change increasing their release and availability at northern latitudes. Currently, the form of mercury known to be most detrimental to human health is methylmercury, CH3Hg+, which is found in the environment and accumulates in the tissues of piscivores, including those consumed by Alaska Natives through subsistence gathering. Much is known about the neurotoxicity of methylmercury after exposure to high concentrations, but little is known about toxicity to other tissues and cell types, particularly for long-term exposure and the lower concentrations that would occur through fish consumption. Effects of methylmercury exposure on 3T3-L1 adipocytes in culture were assessed using assays for cytotoxicity and an ELISA assay for vascular endothelial growth factor (VEGF), a signaling molecule shown to be important for maintaining metabolic status in adipose tissue. Results showed that exposure to methylmercury leads to significant toxicity in adipocytes at exposures of 100 ng/mL during later stages of differentiation, but lower methylmercury concentrations produced little to no toxicity. Results also showed that VEGF secretion is elevated in adipocytes exposed to methylmercury after the process of differentiating into mature, fat-storing cells. These results provide a basis for further exploration into metabolic consequences of methylmercury exposure on specific cell types and cell models.

Pathologic Features of Primary and Metastatic Hepatic Malignancies.

In the mammalian liver, 60 % of the cellular components are hepatocytes while the remainder (35 %) includes biliary epithelium, Kupffer cells, endothelial cells, fat storing cells and connective tissue cells. Although neoplasms of hepatocytes are the most common, a significant number of both benign and malignant primary liver neoplasms arising from other cell types can develop, such as tumors of bile duct epithelium (Table 1). In addition, the liver is one of the most susceptible sites for metastatic tumors arising from other organs of the body. Not too long ago, liver tumors were left untreated because the liver was considered a complex and mysterious organ inaccessible to surgery. Advances in imaging procedures and surgical techniques over the past 40 years have revolutionized the approaches to the treatment of benign and malignant liver tumors. Subsegmentectomy, segmentectomy, lobectomy, and transplantation are routinely performed for the treatment of primary and metastatic liver tumors with minimal morbidity and mortality. Since accurate diagnosis remains the key to clinical and surgical management, the emphasis of this chapter is on classification, morphological features and differential diagnosis of malignant neoplasms of the liver.

White-to-brown metabolic conversion of human adipocytes by JAK inhibition.

The rising incidence of obesity and related disorders such as diabetes and heart disease has focused considerable attention on the discovery of novel therapeutics. One promising approach has been to increase the number or activity of brown-like adipocytes in white adipose depots, as this has been shown to prevent diet-induced obesity and reduce the incidence and severity of type 2 diabetes. Thus, the conversion of fat-storing cells into metabolically active thermogenic cells has become an appealing therapeutic strategy to combat obesity. Here, we report a screening platform for the identification of small molecules capable of promoting a white-to-brown metabolic conversion in human adipocytes. We identified two inhibitors of Janus Kinase (JAK) activity with no precedent in adipose tissue biology that stably confer brown-like metabolic activity to white adipocytes. Importantly, these metabolically converted adipocytes exhibit elevated UCP1 expression and increased mitochondrial activity. We further found that repression of interferon signalling and activation of hedgehog signalling in JAK-inactivated adipocytes contributes to the metabolic conversion observed in these cells. Our findings highlight a novel role for the JAK/STAT pathway in the control of adipocyte function and establish a platform to identify compounds for the treatment of obesity.

Bone Marrow Stromal Cells Inhibit the Activation of Liver Cirrhotic Fat-Storing Cells via Adrenomedullin Secretion.

Cirrhosis, or liver fibrosis, which is mainly triggered by cirrhosis fat-storing cells (CFSCs) activation, has traditionally been considered an irreversible disease. However, recent observations indicate that even advanced fibrosis is still reversible by removing the causative agents. Anti-fibrotic effects of bone marrow-derived stromal cells (BMSCs) have been demonstrated by inhibiting CFSCs via cytokines secretion; however, the mechanisms are still unclear. The purpose of this study was to explore the underlying mechanisms by which BMSCs modulate the function of activated CFSCs. After the co-culture of CFSCs with BMSCs supernatants with or without the addition of recombinant rat adrenomedullin (AM)/AM-specific siRNA, western blot analysis was mainly used to detect the differences of relative protein expression on CFSCs. BMSC-secreted adrenomedullin (AM) effectively inhibited the proliferation and activation of CFSCs by suppressing the expression of Ang II and its binding receptor, AT1, which resulted in a reduction of p47-phox formation. Our data suggested that BMSCs inhibited CFSC activation in vitro via the AM-Ang II-p47-phox signaling pathway, and since CFSC activation is an essential part of hepatic fibrosis process, this inhibition by BMSCs implies us new insights into the potential treatment of hepatic fibrosis via BMSCs.

Extrahepatic bile duct ligation in broiler chickens: ultrastructural study of Ito cell

The Ito cell (fat-storing cell) is a cell lying in perisinusoidal space of liver. The function of Ito cell is expanding from a site of fat-storing site to a center of extracellular matrix metabolism and mediator production in the liver. This study was performed in order to evaluate the Ito cells in cholestatic condition. The artificial cholestatic was conducted by ligation of extrahepatic bile ducts (bile duct ligation = BDL) in broilers. The results showed that BDL induced bile congestion, fibrosis, proliferation of Ito cells and intrahepatic bile ductules. Immunohistochemistry demonstrated that Ito cells were scattered throughout the fibrotic areas, and larger in size with more extensive immunoreactivity than those in normal livers. Ultrastructural study demonstrated that Ito cells were closely associated with the production of extracellular collagen fibers. Ito cells actively react against hepatocytic injuries, especially in fibrogenesis of cholestatic livers. Key words: Bile duct, ito cell, broiler

The effect of lipid metabolism on biological characteristics of hepatic stellate cell

Hepatic stellate cells(HSCs) are a kind of fat-storing cells, the lipid droplets are rich in the Cytoplasm, in which retinyl ester accounts for 42%, triglyceride occupies 28%, cholesterol (total) occupies 13%, phospholipids occupies 4% respectively. Studies have confirmed that thetransforms of HSC phenotype follows the changing of the cell lipid. After the activation of HSC, with HSC phenotype changing from fat-storing cells into myofibroblast, the lipid droplets decreased or disappeared gradually, which means HSCs are under the differentiating process of removing adipose, meawhile triglyceride, and the main content of lipid droplets, also obviously reduced. It was ever declined that during the process of HSC re-fating, the activated HSC would turn into quiescent state. Therefore this shows HSCs fat metabolism is closely related to the biological activity.

Uptake and storage of vitamin A as lipid droplets in the cytoplasm of cells in the lamina propria mucosae of the rat intestine

Vitamin A (retinyl palmitate) was injected subcutaneously or administered to rats by tube feeding. After subcutaneous injection, vitamin A was taken up and stored in cells of the lamina propria mucosae of the rat intestine. After oral administration, vitamin A was absorbed by the intestinal absorptive epithelial cells and transferred to cells of the lamina propria mucosae, where cells took up and stored the transferred vitamin A. The morphology of these cells was similar to that of hepatic stellate cells (also called vitamin A-storing cells, lipocytes, interstitial cells, fat-storing cells or Ito cells). Thus, these cells in the intestine could take up vitamin A from the systemic circulation and as well as by intestinal absorption, and store the vitamin in the lipid droplets in their cytoplasm. The data suggest that these cells are extrahepatic stellate cells of the digestive tract that may play roles in both the absorption and homeostasis of vitamin A.