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White adipose tissue, H&E (lipoma section). Mature unilocular adipocytes with the classic signet-ring appearance: large empty spaces after lipid extraction, thin cytoplasm rims, and peripheral haematoxylin-stained nuclei. Fibrous capsule and septal stroma visible.

Hyeree Kim, Sang Hyun Cho, Jeong Deuk Lee, Hei Sung Kim, Wikimedia Commons · CC BY 4.0

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White adipose tissue, histological section. Unilocular adipocytes in connective tissue context, showing the lobular architecture of adipose tissue and the relationship between fat cells and their supporting stroma.

Berkshire Community College Bioscience Image Library, Wikimedia Commons · CC0

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Brown adipose tissue, histological section. Multilocular adipocytes with smaller lipid droplets and cytoplasm-rich cells, distinct from the unilocular white adipocyte. The denser, more granular cytoplasm reflects the high mitochondrial content that drives UCP1-mediated thermogenesis.

Wikimedia Commons · public domain

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White adipose tissue, H&E (inferred). Adipocytes with lipid voids at the centre and peripheral pink nuclei pushed to the cell rim. Ghost-cell morphology is the expected artifact of paraffin processing: lipid dissolves, leaving a clear sphere outlined by a thin cytoplasmic rim and a flattened crescent nucleus.

Echinaceapallida, Wikimedia Commons · CC BY-SA 4.0

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Perirenal adipose tissue in yak calves (H&E, panels A-B; SEM, Oil Red O and UCP1 IHC, panels C-I). Postnatal day 1 and day 30 sections show multilocular brown adipocytes (black arrows) with smaller lipid droplets and mitochondria-rich cytoplasm, contrasting with the large unilocular white adipocytes in the surrounding depot.

Bai Z, Fan W, Hao L et al. Front Vet Sci. 2026;13:1710538. PMID: 42052336 · CC BY 4.0

PMID 42052336 · fig. Fig 1 A-B

Differentiated adipocytes (PA6 cell line), light microscopy. Round lipid-laden cells with cytoplasm compressed to a thin rim around the central lipid droplet, demonstrating the characteristic unilocular morphology of the white adipocyte.

M. Oktar Guloglu, Wikimedia Commons · CC BY-SA 4.0

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Transmission electron microscopy of dedifferentiated fat (DFAT) cells derived from human adipose tissue. After 7 days of ceiling culture on ACLAR, cells show multiple lipid droplets (L), mitochondria (M), nucleus (N), and collagen (C), demonstrating adipocyte plasticity and return to a progenitor-like state.

Ostinelli G, Gauthier MF, Vernoux N et al. Front Cell Dev Biol. 2025;13:1547836. PMID: 40406419 · CC BY 4.0

PMID 40406419 · fig. FIGURE 1 B

Unilocular and Multilocular adipocytes of adipose tissue from rats. (A) Representative histological images of unilocular adipocytes in brown adipose tissue (BAT) and multilocular adipocytes in inguinal (iWAT) and epididymal (eWAT) adipose tissues. Stain: hematoxylin and eosin. Scale bar: 10 μm (BAT) and 5 μm (iWAT and eWAT); (B) Quantification of unilocular adipocytes in BAT and multilocular adipocytes in iWAT and eWAT. Values are presented as box plots with whiskers from minimum to maximum (n = 5/group). *p < 0.05 effect of diet; # p < 0.05 effect of Tucum-do-Cerrado.

Cavalcanti MH, Damazo AS, Arruda SF. Mol Nutr Food Res. 2026;70(13):e70498. PMID: 42377995 · CC BY 4.0

PMID 42377995 · fig. FIGURE 3

Histological images of adipose tissues of rats. (A) Morphological evaluation of Brown (BAT), inguinal (iWAT), and epididymal (eWAT) adipose tissues. Stain: hematoxylin and eosin. Scale bar: 20 μm (BAT) and 10 μm (iWAT and eWAT). (B) Quantification of unilocular adipocyte area. Values are presented as box plots with whiskers from minimum to maximum (n = 5/group). *p < 0.05 effect of diet; # p < 0.05 effect of Tucum-do-Cerrado.

Cavalcanti MH, Damazo AS, Arruda SF. Mol Nutr Food Res. 2026;70(13):e70498. PMID: 42377995 · CC BY 4.0

PMID 42377995 · fig. FIGURE 2

Human adipose tissue cell, light microscopy from a medical college microbiology class. White adipocytes show the unilocular empty space after lipid extraction with a thin cytoplasm rim and peripheral nucleus.

Chalova.lina, Wikimedia Commons · CC BY 4.0

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Yellow adipose tissue, paraffin section with lipids washed out during processing. The empty round spaces correspond to former lipid droplets dissolved by organic solvents. Thin cytoplasm rims and peripheral nuclei remain. From the Department of Histology, Jagiellonian University Medical College, Krakow.

Department of Histology, Jagiellonian University Medical College, Wikimedia Commons · CC BY-SA 3.0

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White adipose connective tissue, 200x magnification. Cross section showing lobules of unilocular adipocytes surrounded by thin connective tissue septa. From the Berkshire Community College Bioscience Image Library.

Berkshire Community College Bioscience Image Library via Flickr, Wikimedia Commons · CC0

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Lipoblast-like histiocyte in fat necrosis of the breast (H&E). A foamy histiocyte with lightly eosinophilic cytoplasm and a small normochromatic nucleus that is not hollowed out by lipid vacuoles, distinguishing it from a true lipoblast. Olympus LC30, by Mikael Haggstrom, M.D.

Mikael Haggstrom, M.D., Wikimedia Commons · CC0

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During differentiation a myriad of adipogenic loci are under the influence of chromatin modifying complexes. This figure outlines 2 major points of regulation of adipogenesis. b) PPARγ target regulation. PPARγ acts on a variety of genes implicated in adipocyte differentiation and function.

Cook, A. and Cowan, C., Adipose (March 31, 2009), StemBook, ed. The Stem Cell Research Community, StemBook, doi/10.3824/stembook.1.40.1, http://www.stembook.org . · CC BY 3.0

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White adipose tissue, hematoxylin and eosin stain; unilocular adipocytes with peripheral nuclei, fine connective tissue septa

Veeresh likhitha · CC BY-SA 4.0

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adipo-bodipy-ld-1-1.tif

Human adipocytes stained with BODIPY 505/515 (green, lipid droplets) and DAPI (blue, nuclei); fluorescence confocal microscopy

Rkott · CC BY-SA 4.0

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adipo-oil-red-o-1-1.tif

Human adipocytes stained with Oil Red O (red, neutral lipids) and hematoxylin (blue, nuclei); light microscopy

Rkott · CC BY-SA 4.0

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Adipose connective tissue, light micrograph; unilocular white adipocytes with sparse cytoplasm and peripheral nucleus embedded in connective tissue stroma

Berkshire Community College Bioscience Image Library · CC0

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Adipose connective tissue cross-section, light micrograph 200x; unilocular white adipocytes showing signet-ring appearance after lipid extraction during processing

Berkshire Community College Bioscience Image Library · CC0

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Cordycepin comprehensively restores mitochondrial quality control and homeostasis in the brown adipose tissue of mice exposed to constant light. ( A ) Representative transmission electron microscopy (TEM) images showing mitochondrial ultrastructure. Circles highlight damaged mitochondria exhibiting fragmented cristae and vacuolization. Scale bars: 2 um (upper) and 500 nm (lower). ( B ) Quantification of total reactive oxygen species (ROS); ( C ) mitochondrial ROS (mtROS); ( D ) lipid peroxidation product malondialdehyde (MDA); ( E ) total superoxide dismutase (SOD) enzymatic activity; ( F ) relative mitochondrial DNA (mtDNA) copy number; ( G ) total ATP content in BAT homogenates. ( H - J ) relative mRNA expression of genes related to biogenesis (Nrf1, Tfam), mitophagy (Pink1, Parkin) and genes regulating mitochondrial dynamics (Mfn1, Mfn2, Drp1); ( K - O ) representative Western blot and corresponding densitometric quantifications showing protein levels of NRF1, TFAM, total DRP1, and p-DRP1 Ser616 ( K - M ), and markers of mitophagic flux including the LC3-II/LC3-I and p62 degradation ( N , O ). Tubulin was used as a loading control for Western blots. Data are presented as mean +/- SD with individual data points shown (n = 6 mice per group for physiological and molecular assays; n = 3 mice per group for Western blot). Statistical significance was determined by one-way ANOVA followed by Tukey's post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001).

Bi, Zhang, Wang et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42196331 · fig. Figure 4

E4BP4 prevents obesity-induced mitochondrial fragmentation. (A) Transmission electron microscopy (TEM) of mitochondrial morphology in iBAT at 28-29 degrees C in Control and E4BP4-OE mice after 10 weeks of HFD feeding. Representative image. Scale bar: 2 um. Red arrows show mitochondria. (B) Kernel density plot of maximal mitochondrial length of (A). (C) Quantification of maximal mitochondrial length (n = 3 per group). Data were presented as mean +/- SEM. (D) Schematic illustration of experimental design for (E). (E) Right: Images of mitochondrial morphology in primary brown adipocytes by TOM20 immunofluorescence after 24 h of control treatment (BSA) or palmitate stimulation (BSA:PAL). Representative image. Scale bar, 10 um. Left: Quantification of cells with a fragmented mitochondrial network (n = 4; 100-220 mitochondria from ten images/group/experiment). Data were presented as mean +/- SEM. (G) Left: live-cell fluorescence of MitoDendra2 in primary brown adipocytes infected with AAV-control or E4BP4. Representative image. Scale bar, 12 um. Right: Quantification of colocalization of Dendra active and not-activated. Data were presented as mean +/- SEM. (H) Oxygen consumption rate (OCR) in differentiated primary brown adipocytes expressing Control or E4bp4 after pretreatment for 6 h with control treatment (BSA) or palmitate stimulation (BSA:PAL).

Valdivieso-Rivera, Furino, Leher et al 2026, EMBO Reports · CC BY 4.0

PMID 42332066 · fig. Figure 3

BIX02189 suppresses adipocyte differentiation and lipid accumulation in 3T3-L1 cells in a dose-dependent manner. (A) Representative phase-contrast and Oil Red O-stained images of 3T3-L1 cells. Preadipocytes (D0) were induced to differentiate and treated with BIX02189 (0, 5, 10, and 20 uM) throughout the differentiation period (D0-D8). Control cells exhibited extensive lipid droplet formation, whereas BIX02189 treatment reduced lipid accumulation in a concentration-dependent manner. (B) Quantitative analysis of intracellular triglyceride (TG) content in differentiated 3T3-L1 adipocytes. TG levels were significantly decreased following BIX02189 treatment in a dose-dependent manner. (C) Cell viability of 3T3-L1 cells treated with BIX02189 for 8 days. Cell survival was expressed as a percentage of the control group. BIX02189 at 5 and 10 uM had minimal effects on cell viability, whereas a moderate reduction was observed at 20 uM. Data are presented as mean +/- SE from at least three independent experiments. * p < 0.05 versus control.

Perumal, Hussain, Son et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 42511811 · fig. Figure 2

Deficiency of Ccr1 increases adaptive thermogenesis of cold-stimulated mice. (A) Relative mRNA expression of Ccr1 in the adipose tissues of 4°C-stimulated mice (n = 4). (B) Rectal temperature of mice (n = 4). (C) Uncoupling protein 1 (UCP1)-stained brown adipose tissue (BAT) sections of mice (n = 4). Scale bars = 100 um. (D) Immunoblots of UCP1, p-PKA-C and p-CREB and their total proteins in BAT of 4°C-stimulated mice (n = 4). (E) Relative mRNA levels of thermogenic genes in BAT of mice (n = 4). (F) UCP1-stained inguinal white adipose tissue (iWAT) sections of mice (n = 4). Scale bars = 100 um. (G) Immunoblots of UCP1, p-PKA-C and p-CREB and their total proteins in iWAT of mice (n = 4). (H) Relative mRNA levels of thermogenic genes in iWAT of 4°C-stimulated mice (n = 4). Data are presented as mean +/- SEM. (B-H) Two-tailed Student's t-test. *p < .05, **p < .01.

Cai, Ma, Zhu et al 2026, Clinical and Translational Medicine · CC BY 4.0

PMID 42557944 · fig. FIGURE 4

Confocal analysis of visceral adipose tissue from rats with MASLD treated with CDPs. ( A ) Representative confocal microscopy images of visceral adipose tissue sections stained with Propidium Iodide (PI), MitoTracker Green, and anti-UCP1 antibody, with clear-field images shown (20x magnification). Scale bar = 50 um. Animal groups are defined in Figure 2 . ( B ) Quantification of fluorescence intensity using MitoTracker Green staining and UCP1 immunodetection. VAT samples from six animals per animal group ( n = 6) were dissected and processed for staining. Fifteen representative microscopic fields acquired from the six animals in each experimental group were analyzed to quantify fluorescence. Bars represent the means +/- SEM, n = 6 animals per group. Statistical analysis was performed using one-way ANOVA, followed by Tukey's post hoc test. Different lowercase letters indicate significant differences ( p < 0.05).

Figueroa-Guzman, Campos-Morales, Martinez-Alcantar et al 2026, Molecules · CC BY 4.0

PMID 42513149 · fig. Figure 8

MAM-LD architecture is strongly altered in the inguinal adipose tissue of Seipin-deficient mice. ( A - D ) Inguinal adipose tissue was collected from Bscl2 (Control) and lox/lox Bscl2 lox/lox ERT2-Adipoq-Cre (iATSKO) mice in the random-fed state, 14 days after tamoxifen injection (100 mg/kg). Transmission electron microscopy (TEM) images were analyzed, and the contact surface areas of mitochondria-associated membranes (MAMs), mitochondria-lipid droplet (Mi-LD), and endoplasmic reticulum-lipid droplet (ER-LD) interfaces were quantified using Fiji, as described in the Materials and Methods. ( E - F ) MAM subpopulations were quantified according to their proximity to lipid droplets: MAM-LD (<50 nm from LDs) and MAM-CM (>50 nm from LDs). ( G, H ) MAM abundance was quantified using proximity ligation assay (PLA) for IP3R and VDAC, combined with PLIN1 immunofluorescence and structured illumination microscopy (SIM). Representative images show PLIN1 (gray), MAM-LD (magenta), and MAM-CM (pink) ( G ). Total PLA signals were quantified and classified according to their distance from lipid droplets: MAM-LD (<380 nm from LDs) and MAM-CM ( >380 nm from LDs) ( H ). ( I ) Representative focused ion beam-scanning electron microscopy (FIB-SEM) images of adipose tissue sections from Control and iATSKO mice. Organelle segmentation shows mitochondria (orange), lipid droplets (yellow), nucleus (blue), and plasma membrane (white). ( J - M ) Cryopreserved subcutaneous adipose tissue from Control and iATSKO mice in the fed or 18 h fasted state was analyzed by PLIN1 immunofluorescence ( J ). PLA was used to quantify MAMs (VDAC/IP3R; K ), Mi-LD contacts (PTPIP51/PLIN1; L ), and ER-LD contacts (VAPB/PLIN1; M ). ( N, O ) Lipid droplets were isolated from Control and iATSKO mice and subjected to lipidomic analysis.

Palard, Chadeuf, Carpentier et al 2026, The EMBO Journal · CC BY 4.0

PMID 42487075 · fig. Figure 1

MAM-LD architecture is strongly altered in the inguinal adipose tissue of Seipin-deficient mice. (A-D) Inguinal adipose tissue was collected from Bscl2 lox/lox (Control) and Bscl2 lox/lox ERT2-Adipoq-Cre (iATSKO) mice in the random-fed state, 14 days after tamoxifen injection (100 mg/kg). Transmission electron microscopy (TEM) images were analyzed, and the contact surface areas of mitochondria-associated membranes (MAMs), mitochondria-lipid droplet (Mi-LD), and endoplasmic reticulum-lipid droplet (ER-LD) interfaces were quantified. (E-F) MAM subpopulations were quantified according to their proximity to lipid droplets: MAM-LD (< 50 nm from LDs) and MAM-CM (> 50 nm from LDs). (G, H) MAM abundance was quantified using proximity ligation assay (PLA) for IP3R and VDAC, combined with PLIN1 immunofluorescence and structured illumination microscopy (SIM). Representative images show PLIN1 (gray), MAM-LD (magenta), and MAM-CM (pink) (G). (I) Representative focused ion beam-scanning electron microscopy (FIB-SEM) images of adipose tissue sections from Control and iATSKO mice. Organelle segmentation shows mitochondria (orange), lipid droplets (yellow), nucleus (blue), and plasma membrane (white). (J-M) Cryopreserved subcutaneous adipose tissue from Control and iATSKO mice in the fed or 18 h fasted state was analyzed by PLIN1 immunofluorescence (J). PLA was used to quantify MAMs (VDAC/IP3R; K), Mi-LD contacts (PTPIP51/PLIN1; L), and ER-LD contacts (VAPB/PLIN1; M).

Palard, Chadeuf, Carpentier et al 2026, The EMBO Journal · CC BY 4.0

PMID 42487075 · fig. Figure 1

The HUVAS culture model facilitates the differentiation of unilocular human white adipocytes in vitro. A: Schematic of 2D, scaffold-free 3D, and scaffolded HUVAS cultures, done side by side using stromal vascular fraction cells from same donor and passage, cultured in the same media and with the same differentiation time, varying only the cell environment. B: Representative confocal images of BODIPY, CellMask, and DAPI-stained adipocytes on day (d)30. Scale bars for all images in Figure 1: 500 um (main), 50 um (inset). C-F: Quantification of lipid droplet diameter (C), total lipid droplet area (D), adipocyte unilocularity (E), and total adipocyte area (F) across isogenic 2D, 3D, and HUVAS cultures from n = 50 cells per spheroid and 3 spheroids per individual. Similar results were obtained from cells from three different cell donors.

Maestri, Cai, Schipper et al 2026, Journal of Lipid Research · CC BY 4.0

PMID 41850682 · fig. Fig. 1

(a) Adipocyte nucleus (N) with a pronounced nucleolus (nu) without indentation in non-lipedema control tissue (sagittal plane). The nucleus appears flat, adapting its form to the curvature of the mature adipocyte and is closely attached to the main lipid droplet (mLD). (b) Lochkern in a lipedema adipocyte (sagittal plane). The bulging of the nucleus, due to the indentation, is seen. Electron optical analysis clearly indicates that the content of the satellite droplet (SD) and the mLD is identical (asterisks). (c) Ultrathin sections showing the contact zone between the nucleus and the SD at the nuclear pore (arrowheads). A mitochondrion is seen within the adipocyte cytoplasm (m). (d) A channel-like stucture connects the SD with the adjacent heterochromatin (arrow) and the nuclear pore contact (arrowhead). (e) High magnification of a strongly extended contact region [462 nm, measured by ImageJ] between a satellite droplet and the nuclear membrane. (f) A Lochkern showing a fenestration for passage of the satellite droplet to the main droplet. Black arrows indicate the opening within the nuclear membrane, white arrowheads point to the dissolution of the phosholipid membrane. (g) A lateral small lipid droplet is fusing (black arrow) with the large satellite droplet. This fusion process (arrowheads) is identical with fusion of normally generated LDs during lipogenesis.

Steiner, Rinnerthaler, Mueller et al 2026, Frontiers in Cell and Developmental Biology · CC BY 4.0

PMID 42148303 · fig. FIGURE 4

MAM-LD architecture is strongly altered in the inguinal adipose tissue of Seipin-deficient mice. (A-D) Inguinal adipose tissue was collected from Bscl2lox/lox (Control) and Bscl2lox/lox ERT2-Adipoq-Cre (iATSKO) mice in the random-fed state, 14 days after tamoxifen injection (100 mg/kg). Transmission electron microscopy (TEM) images were analyzed, and the contact surface areas of mitochondria-associated membranes (MAMs), mitochondria-lipid droplet (Mi-LD), and endoplasmic reticulum-lipid droplet (ER-LD) interfaces were quantified. (E-F) MAM subpopulations were quantified according to their proximity to lipid droplets: MAM-LD (<50 nm from LDs) and MAM-CM (>50 nm from LDs). (G, H) MAM abundance was quantified using proximity ligation assay (PLA) for IP3R and VDAC, combined with PLIN1 immunofluorescence and structured illumination microscopy (SIM). Representative images show PLIN1 (gray), MAM-LD (magenta), and MAM-CM (pink) (G). (I) Representative focused ion beam-scanning electron microscopy (FIB-SEM) images of adipose tissue sections from Control and iATSKO mice. Organelle segmentation shows mitochondria (orange), lipid droplets (yellow), nucleus (blue), and plasma membrane (white). (J-M) Cryopreserved subcutaneous adipose tissue from Control and iATSKO mice in the fed or 18 h fasted state was analyzed by PLIN1 immunofluorescence (J). PLA was used to quantify MAMs (VDAC/IP3R; K), Mi-LD contacts (PTPIP51/PLIN1; L), and ER-LD contacts (VAPB/PLIN1; M).

Palard, Chadeuf, Carpentier et al 2026, The EMBO Journal · CC BY 4.0

PMID 42487075 · fig. Figure 1

Agnuside reinforces mitochondrial respiratory complex assembly and cristae architecture in thermogenic adipose tissue. (A) Heatmap of protein abundance in BAT from mice exposed to acute cold (4 degrees C, 5 h). Eight-week-old male C57BL/6J mice received daily intraperitoneal injections of AGN (7.5 mg/kg) for 4 weeks before cold exposure. Proteomic data were z-score-normalized and visualized as heatmaps ( n = 4 per group). (B) Representative transmission electron microscopy (TEM) images of BAT mitochondria from mice treated as in (A). Scale bar, 2 um. (C,D) Quantification of mitochondrial diameter (C) and cristae abundance (D) from TEM images shown in (B). n = 300 mitochondria each group in (C), and n = 80 mitochondria each group in (D). (E) ATP content in BAT tissues from mice treated as in (A) ( n = 5 per group). (F) Western blot analysis of representative subunits of mitochondrial respiratory complexes in BAT from mice treated as in (A), with densitometric quantification on the right ( n = 4 per group). (G) Blue native-PAGE (BNPAGE) analysis of isolated BAT mitochondria from mice in (A), with quantification of respiratory complexes shown below ( n = 3 per group). (H,J) Western blot analysis of representative subunits of mitochondrial respiratory complexes in BAT (H) and iWAT (J) from HFD-fed mice treated with AGN, with quantification shown on the right ( n = 4 per group). (I,K) BN-PAGE analysis of mitochondria isolated from BAT (I) and iWAT (K) from HFD-fed mice treated with AGN, with quantification shown on the right ( n = 3 per group). Data, except for panels (A,C,D), are presented as mean +/- SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Zhao, Xie, Wang et al 2026, Advanced Science · CC BY 4.0

PMID 42299748 · fig. FIGURE 4

Orai1 deficiency impairs mitochondrial Ca2+ uptake and structural remodelling during thermogenic activation. (a) Model illustrating that cold-induced Ca2+ influx via Orai1 is essential for mitochondrial Ca2+ uptake and subsequent thermogenesis. (b) Rhod-2 fluorescence imaging of mitochondrial Ca2+ in siCtrl and siOrai1 cells. (c) Quantification of mitochondrial Ca2+ uptake following temperature shifts (37 degrees C to 15 degrees C). (d) Transmission electron microscopy images of BAT from control and brown adipocyte-specific Orai1 knockout (BKO) mice exposed to cold for 6 h. (e) Western blot analysis of oxidative phosphorylation proteins in control and Orai1 BKO brown adipose tissue after cold exposure (4 degrees C) for 6 h. (f) Western blot analysis of oxidative phosphorylation proteins during differentiation of preadipocytes to brown adipocytes treated with siOrai1. (g) Mitochondrial DNA copy number measured in control and Orai1-deficient cells with CL316243 treatment. (h) Oxygen consumption rate (OCR) analysis of Orai1-deficient adipocytes treated with CL316243. (i) Fatty acid oxidation (FAO) assay of Orai1-deficient adipocytes treated with CL316243. Data are presented as mean +/- SEM. Statistical significance *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. FCCP, carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone; FFA, free fatty acid; ns, not significant.

Kim, Nguyen, Park et al 2026, Experimental and Molecular Medicine · CC BY 4.0

PMID 42595867 · fig. Fig. 5

Analysis of endogenous PLINs in human adipocyte (TERT-hWA) cultures suggests different modes of interaction with LDs. (A) Time course of adipocyte differentiation. (B) Western blot analysis of adipocyte markers and PLINs during adipocyte differentiation. P: proliferation; D3, D6, and D11: day of differentiation. (C) Representative z sections obtained by confocal fluorescence microscopy of endogenous PLIN1 (blue), PLIN2 (red), and PLIN4 (green) in human adipocytes at day 10 of differentiation after immunofluorescence with specific antibodies, with the nuclei stained with DAPI (white). Bottom panels show the three protein channels in the indicated area. The cells were maintained in culture medium or fed with 100 uM oleic acid for 2.5 h before observation. Scale bar: 10 um. (D) Quantification showing the fraction of cells with PLIN4 signal as indicated under the same conditions as in C. Four categories were defined: cells without detectable PLIN4; cells in which PLIN4 was entirely cytosolic; cells in which PLIN4 was mostly cytosolic but marked a few puncti (possible LDs); cells in which PLIN4 was LD-localized. N of cells quantified was 108 for D3 - OA, 104 for D3 + OA, 92 for D6 - OA, 92 for D6 + OA, 98 for D10 - OA and 93 for D10 + OA, from one of two representative experiments.

Dias Araujo, Bello, Bigay et al 2024, The Journal of Cell Biology · CC BY 4.0

PMID 39297796 · fig. Figure 1

Immunofluorescence localization of PLIN1 on LDs in perirenal adipose tissue of 1- and 30-days-old yak calves: (A-C) Perirenal adipose tissue at 1 day old; (D-F) Perirenal adipose tissue at 30 days old; (G-I) Negative controls. White arrows indicate PLIN1-positive on LD in adipocytes, red arrows indicate nuclei of PLIN1-positive adipocytes. Scale bars: 10 um.

Bai, Fan, Hao et al 2026, Frontiers in Veterinary Science · CC BY 4.0

PMID 42052336 · fig. Figure 3

WD enhances nuclear localization of SPHK2 in SWAT. ( A ) Representative confocal micrographs of sWAT from 18 week chow or WD fed Sphk2 DeltaAdipo and WT male mice were stained for SPHK2 and counterstained with DAPI and then quantified ( B ) as % SPHK2-stained area per nuclei ( N = 6, n = 8). Data are presented as means +/- SEM; **** P <= 0.0001 compared with WT littermates fed chow diet, unpaired two-tailed t test. ( C ) Representative confocal micrographs of sWAT, gWAT, and BAT from WT mice stained for SPHK2 or UCP1 and counterstained with DAPI and were quantified ( D ) as % SPHK2-stained area per nuclei or as % UCP1-stained area per field ( N = 4, n = 8). ( E ) Chromatin fractions from WT primary white adipocytes were separated by SDS-polyacrylamide gel electrophoresis (PAGE) and immunoblotted with SPHK2-specific antibody. Antibodies against histone H3 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were used as markers for chromatin and cytosol. ( F ) Representative immunofluorescence images of WT or Sphk2 knockout (KO) primary adipocytes treated with vehicle or palmitate (500 uM) for 24 hours and were quantified ( G ) as % SPHK2-stained area per nuclei ( N = 6, n = 8). Scale bars, 5 um.

Brown, Weigel, Vijayan et al 2026, Science Advances · CC BY 4.0

PMID 42627910 · fig. Fig. 8

WD enhances nuclear localization of SPHK2 in SWAT. (A) Representative confocal micrographs of sWAT from 18 week chow or WD fed Sphk2 DeltaAdipo and WT male mice were stained for SPHK2 and counterstained with DAPI and then quantified (B) as % SPHK2-stained area per nuclei (N = 6, n = 8). (C) Representative confocal micrographs of sWAT, gWAT, and BAT from WT mice stained for SPHK2 or UCP1 and counterstained with DAPI and were quantified (D) as % SPHK2-stained area per nuclei or as % UCP1-stained area per field (N = 4, n = 8). (F) Representative immunofluorescence images of WT or Sphk2 knockout (KO) primary adipocytes treated with vehicle or palmitate (500 uM) for 24 hours and were quantified (G) as % SPHK2-stained area per nuclei (N = 6, n = 8). Scale bars, 5 um.

Brown, Weigel, Vijayan et al 2026, Science Advances · CC BY 4.0

PMID 42627910 · fig. Fig. 8.

WD enhances nuclear localization of SPHK2 in SWAT. (A) Representative confocal micrographs of sWAT from 18 week chow or WD fed Sphk2 DeltaAdipo and WT male mice were stained for SPHK2 and counterstained with DAPI and then quantified (B) as % SPHK2-stained area per nuclei (N = 6, n = 8). Data are presented as means +/- SEM; **** P <= 0.0001 compared with WT littermates fed chow diet, unpaired two-tailed t test. (C) Representative confocal micrographs of sWAT, gWAT, and BAT from WT mice stained for SPHK2 or UCP1 and counterstained with DAPI and were quantified (D) as % SPHK2-stained area per nuclei or as % UCP1-stained area per field (N = 4, n = 8). (E) Chromatin fractions from WT primary white adipocytes were separated by SDS-PAGE and immunoblotted with SPHK2-specific antibody. Antibodies against histone H3 and GAPDH were used as markers for chromatin and cytosol, respectively. (F) Representative immunofluorescence images of WT or Sphk2 knockout (KO) primary adipocytes treated with vehicle or palmitate (500 uM) for 24 hours and were quantified (G) as % SPHK2-stained area per nuclei (N = 6, n = 8). Scale bars, 5 um.

Brown, Weigel, Vijayan et al 2026, Science Advances · CC BY 4.0

PMID 42627910 · fig. Fig. 8.

Cold Exposure Induces Subcellular Structural Changes in the Inguinal Adipose Tissue of Pigs. ( A , B ) Scanning electron microscopy images of the cold exposure and control groups, with the green arrows indicating multilocular lipid droplets in adipocytes and the purple arrows indicating blood vessels or lymphatic vessels. ( C - G ) Transmission electron microscopy images of the cold exposure and control groups. ( E ) A typical brown adipocyte showing multiple small lipid droplets within the cell and a greater number of mitochondria. ( C , G ) are close-ups of ( E ). ( D ) is a close-up of ( F ). The orange arrows indicate mitochondria.

Guo, Lv, Ma et al 2025, International Journal of Molecular Sciences · CC BY 4.0

PMID 41155166 · fig. Figure 4

CT increased UCP1 expression in iWAT and rpWAT after 8 weeks. (A) Representative immunohistochemistry images of UCP1 staining in iWAT and rpWAT; (B) UCP1 positive-staining area per field (um2) in each adipose tissue depot; and (C) Multilocular adipocyte area normalized to the total WAT area analyzed. Data are presented as mean +/- SD. Comparisons between SED and CT were performed using an unpaired two-tailed Student's t-test. *p < 0.05 versus the corresponding SED group. Scale bars, 50 um. Abbreviations: SED, sedentary (n = 5 animals); CT, combined training (n = 5 animals); WAT, white adipose tissue; iWAT, inguinal white adipose tissue; rpWAT, retroperitoneal white adipose tissue; UCP1, uncoupling protein 1.

Picoli, Gilio, Henriques et al 2026, Journal of Physiology and Biochemistry · CC BY 4.0

PMID 42753033 · fig. Fig. 5

H&E staining of white adipose tissue from a murine heart failure model. Large unilocular adipocytes with peripheral flattened nuclei are clearly visible. Section from vehicle-treated control animals.

Ma D 2023, Lipids in health and disease · CC BY 4.0

PMID 36670439

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