Fat Cell Formation Research Articles

Simultaneous Effect of Eight Weeks High-fat Diet, Continuous Moderate-intensity Training, and High-intensity Intermittent Training on the Gene Expression Levels of PLIN2 and ATGL in the Twin Muscle of Male Wistar Rats

Background: A high-fat diet can cause obesity and endanger health. Therefore, the present study aimed to investigate the effect of eight weeks of high-fat diet, continuous moderate-intensity training, and high-intensity intermittent training on the gene expression levels of PLIN2 and ATGL in the twin muscles of male Wistar rats. Materials and Methods: Thirty-two male Wistar rats were divided into four groups (n=8): 1- control group with a standard diet (ND) 2- control group with a high-fat diet (HFD) 3- high-fat diet and continuous aerobic training with Moderate intensity (HFD+MICT) 4- high-fat diet and intermittent aerobic training (HFD+HIIT). For one training group, eight weeks of moderate-intensity continuous aerobic training (MICT), and for the other group, eight weeks of high-intensity intermittent aerobic training (HIIT) were performed on the treadmill. Then, 48 hours after the last training session, the twin muscle tissue was isolated to check the expression of PLIN2 and ATGL genes. Gene expression analysis was done by Real-time PCR technique. One-way analysis of variance (ANOVA) and Tukey's post-hoc test were used to analyze the collected data. Results: After eight weeks of training, the level of PLIN2 gene expression in the two training groups was significantly lower than in the HDF group, and the level of ATGL gene expression was significantly higher in both groups than in the HDF group (P<0.05). Conclusion: It was shown that two exercises had a modulating effect on the expression of genes that are effective in the process of autophagy and the formation of fat cells.

Exploring the Interplay between Bone Marrow Stem Cells and Obesity.

Obesity, a complex disorder with rising global prevalence, is a chronic, inflammatory, and multifactorial disease and it is characterized by excessive adipose tissue accumulation and associated comorbidities. Adipose tissue (AT) is an extremely diverse organ. The composition, structure, and functionality of AT are significantly influenced by characteristics specific to everyone, in addition to the variability connected to various tissue types and its location-related heterogeneity. Recent investigation has shed light on the intricate relationship between bone marrow stem cells and obesity, revealing potential mechanisms that contribute to the development and consequences of this condition. Mesenchymal stem cells within the bone marrow, known for their multipotent differentiation capabilities, play a pivotal role in adipogenesis, the process of fat cell formation. In the context of obesity, alterations in the bone marrow microenvironment may influence the differentiation of mesenchymal stem cells towards adipocytes, impacting overall fat storage and metabolic balance. Moreover, bone marrow's role as a crucial component of the immune system adds another layer of complexity to the obesity-bone marrow interplay. This narrative review summarizes the current research findings on the connection between bone marrow stem cells and obesity, highlighting the multifaceted roles of bone marrow in adipogenesis and inflammation.

Non-monotonic dose-response of di-(2-ethylhexyl) phthalate isolated from Penicillium citrinum XT6 on adipogenesis and expression of PPARγ and GLUT4 in 3T3-L1 adipocytes.

Adipogenesis is the fat cell formation process regulated by peroxisome proliferator-activated receptors (PPARγ). The insulin-responsive glucose transporter 4 (GLUT4) has a major role in glucose uptake and metabolism in insulin target tissues (i.e.,adipose and muscle cells). The interplay between PPARγ and GLUT4 is essential for proper glucose homeostasis. This study aimed to isolate, elucidate, and investigate the effect of an isolated compound from Penicillium citrinum XT6 on adipogenesis, PPARγ, and GLUT4 expression in 3T3-L1 adipocytes. The isolated compound was determined by analyzing spectroscopic data (LC-MS, FT-IR, Spectrophotometry UV-Vis, and NMR). The adipogenesis activity of the isolated compound in 3T3-L1 cells was determined by the Oil Red O staining method. RT-PCR was used to analyze the gene expression of PPARγ and GLUT4. Di-(2-ethylhexyl)-phthalate (DEHP) was the isolated compound from P.citrinum XT6. The results revealed adipogenesis stimulation and inhibition, as well as PPARγ and GLUT4 expressions. DEHP showed a non-monotonic dose-response (NMDR) effect on adipogenesis and PPARγ and GLUT4 expression. It is the first study that reveals DEHP's NMDR effects on lipid and glucose metabolism in adipocytes.

Platelet-Rich Plasma: Applications in Cosmetic Dermatology

Platelet-rich plasma (PRP) or autologous platelet gel, plasma-rich growth factors, and platelet-concentrated plasma are blood component that is rich in thrombocytes on a small volume of plasma. There were seven primary growth factors that actively secreted by thrombocytes including platelet-derived growth factor, transforming growth factor-β, vascular endothelial growth factor, epidermal growth factor, fibroblast growth factor, connective tissue growth factor, and insulin-like growth factor-1. PRP application in cosmetic dermatology includes tissue regeneration, wound healing, repairing scar tissue, skin rejuvenation, and being used in alopecia patients. PRP could accelerate soft-tissue formation in the subdermal, activate fibroblast formation and new collagen deposition, and formation of blood vessels and fat cells. PRP is also considered a potential therapy for accelerating hair growth for alopecia.

Extracts from plastic products induce fat-cell formation in cell culture

Extracts from plastic products induce fat-cell formation in cell culture

The Role of Transcription Factors in Chronic Adipose Tissue Inflammation

A transcription factor known as Early B-Cell Factor 1 (EBF1) is key to the formation of fat cells, called adipocytes. Although it is also active in mature adipocytes, the function of EBF1 at this stage has been unclear. Dr Michael Griffin at Sam Houston State University in Texas is investigating how EBF1 is involved in the process of adipose tissue inflammation caused by obesity. This type of inflammation is believed to be the underlying cause of a multitude of diseases ranging from diabetes to cancer.

Self-nanoemulsifying Delivery of Andrographolide: Ameliorating Islet Beta Cells and Inhibiting Adipocyte Differentiation.

Purpose: Insulin resistance is a characteristic of non-insulin-dependent diabetes mellitus associated with obesity and caused by the failure of pancreatic beta cells to secrete sufficient amount of insulin. Andrographolide (AND) improves beta-cell reconstruction and inhibits fat-cell formation. This research aimed to improve the delivery of water-insoluble AND in self-nanoemulsifying (ASNE) formulation, tested in streptozotocin (STZ)-induced diabetic rats and 3T3-L1 preadipocyte cells. Methods: A conventional formulation of AND in suspension was used as a control. The experimental rats were orally administered with self-nanoemulsifying (SNE) and suspension of AND for 8 days. Measurements were performed to evaluate blood glucose levels in preprandial and postprandial conditions. Immunohistochemistry was used to assess the process of islet beta cell reconstruction. In vitro study was performed using cell viability and adipocyte differentiation assay to determine the delivery of AND in the formulation. Results: ASNE lowered blood glucose levels (day 4) faster than AND suspension (day 6). The histological testing showed that ASNE could regenerate pancreatic beta cells. Therefore, ASNE ameliorated pancreatic beta cells. The in vitro evaluation indicated the inhibition of adipocyte differentiation by both AND and ASNE, which occurred in a time-dependent manner. ASNE formulation had better delivery than AND. Conclusion: ASNE could improve the antidiabetic activity by lowering blood glucose levels, enhancing pancreatic beta cells, and inhibiting lipid formation in adipocyte cells.

Probe into the Target and Mechanism of Jianpi Xiaoke Prescription for Treating Type 2 Diabetes Mellitus through miRNA Expression Profiling.

Methods Ten of the 31 SPF male Wistar rats were randomly taken as the control group; the remaining rats were fed a high-sugar and high-fat diet, combined with Streptozotocin (STZ, 35 mg/kg) that induced a type 2 diabetes model. The model rats were randomly divided into model groups (n = 11) and the JPXK group (n = 10). After 8 weeks of JPXK intervention, we detected the function of islet cells through HE staining and ELISA. High-pass sequencing technology was adopted to identify the differential expression of miRNA to explore the target of JPXK treatment, assess the relevant target genes, conduct functional analysis, and lastly verify the sequencing data by qRT-PCR. Results After treatment, FPG, FINS, and HOMA-IR levels of the treatment group improved significantly compared with those of the control group (P < 0.05). Among the miRNAs differentially expressed between the model group and the control group, there were 7 reversals after JPXK treatment, including miR-1-3p, miR-135a-5p, miR-181d-5p, miR-206-3p, miR-215, miR-3473, and miR-547-3p (log2FC ≥ 1 or ≤ −1, P < 0.05). Besides, the 1810 target genes associated with these 7 miRNAs were assessed by multiMiR. According to the results of the GO and KEGG analyses, they were associated with biological processes (e.g., glucose transport and fat cell formation), and it covered multiple signaling pathways, capable of regulating islet cell function (e.g., MAPK, PI3K-Akt, Ras, AMPK, and HIF-1 signaling pathways). The PCR verification results were consistent with the sequencing results. Conclusion This discovery interpreted the potential therapeutic targets and signaling pathways of JPXK prescription against T2DM based on miRNA expression profiling. In conclusion, our research provided novel research insights into traditional Chinese medicine (TCM) treatment of diabetes.

Rosiglitazone-induced changes in the oxidative stress metabolism and fatty acid composition in relation with trace element status in the primary adipocytes.

BackgroundMetabolic syndrome, obesity and type 2 diabetes are metabolic disorders characterized by the insulin resistance and the impairment in the insulin secretion. Since impairment in the oxidative stress and adipocyte metabolism contribute to the formation of obesity and diabetes, targeting adipose tissue can be considered as an effective approach to fight against them. Rosiglitazone is used for treatment for patients with type 2 diabetes via inducing lipogenesis and transdifferentiation of white adipose tissue into brown adipose tissue. Since the development of such therapeutics is required to control the formation and function of brown fat cells, we aimed to reveal possible molecular mechanisms behind rosiglitazone induced biochemical changes in the adipose tissue.MethodsCells were expanded in the adipocyte culture medium supplemented with 5 µg/mL insulin following 2 days' induction. After those cells were treated with rosiglitazone 0, 0.13 mol/L and 10 µmol/L rosiglitazone for 48 hours and at 8th day, cells were collected and stored at -80 °C. Then the cells were used to evaluate antioxidant enzyme activities, mineral and trace element levels and fatty acid composition.ResultsGlucose-6-phosphate dehydrogenase and glutathione reductase significantly reduced in rosiglitazone-treated groups compared to the control. Na, Mg, K, Ca, Cr, Fe, Ni, Cu, Zn, Rb, Sr, Cs, Ba and Pb were determined in the cell lysates via ICP-MS. Also, relative FAME content decreased in the rosiglitazone-treated groups compared to the control.ConclusionsRosiglitazone treatment at low doses showed promising results which may promote brown adipose tissue formation.

Red Raspberry Polyphenols Reduce the High Fat Diet-driven Adipocyte Hypertrophy by Suppressing NLRP3 Inflammasome Activation (P08-028-19)

ObjectivesNLRP3 inflammasome is an innate immune machinery for caspase-1 cleavage and IL-1β secretion. Activation of the NLRP3 inflammasome is a metabolic culprit linking adipose inflammation to systemic metabolic dysfunction. Red raspberry (RR) is rich in polyphenols shown to exert protective role against obesity and metabolic syndrome. This study aimed to investigate the impact of RR polyphenols on activation of NLRP3 inflammasome and its metabolic benefits. MethodsThe whole, seed, and pulp RR polyphenols were fractionated and lyophilized. C57BL/6 male mice were assigned 1 of 5 diets of LF (10% total calorie from fat), HF (45% calorie from fat), or HF diet containing RR polyphenols from whole (0.4%), pulp (0.3%) and seed (0.1%) fraction for 12 weeks. Macrophage infiltration and NLRP3 inflammasome activation were determined by macrophage signature gene/protein expression and caspase-1 cleavage in the epididymal fat and stromal vascular fraction. Adipogenic potential was evaluated by epigenetic marks of H3K27Ac in the stromal vascular fraction. IL-1β reporter assay was used to validate the NLRP3 inflammasome activation in vitro. To explore the paracrine effects of IL-1β in regulating adipogenesis, we designed the conditioned medium experiments between macrophages and C3H10T1/2 murine pluripotent stem cells. ResultsThe whole and pulp, but not seed, RR polyphenols significantly reduced the HF-driven weight gain, dyslipidemia, and insulin resistance. Whole or pulp RR polyphenols decreased inflammation, macrophage recruitment, and adipocyte size in epididymal fat compared to HF alone or seed polyphenols. Reduced adipocyte size by whole and pulp polyphenols was linked with 1) reduced NLRP3 inflammasome in the stromal vascular fraction, evidenced by reduced IκBα degradation and caspase-1 cleavage, and 2) augmented new fat cell formation via epigenetic modifications for adipogenesis (i.e., H3K27Ac, H3K9Ac, and H3K4m2). Supporting these in vivo results, RR polyphenol treatment in macrophages not only attenuated IL-1β reporter assay but also reversed the paracrine action of IL-1β in blocking adipogenesis in vitro. ConclusionsBlocking NLRP3 by RR polyphenols is a promising dietary intervention strategy to promote healthy adipose remodeling, preventing adipocyte hypertrophy, fatty acid spillover, and further metabolic complications. Funding SourcesUSDA NIFA.

Thy1 (CD90) expression is regulated by DNA methylation during adipogenesis.

The obesity epidemic is developing into the most costly health problem facing the world. Obesity, characterized by excessive adipogenesis and enlarged adipocytes, promotes morbidities, such as diabetes, cardiovascular disease, and cancer. Regulation of adipogenesis is critical to our understanding of how fat cell formation causes obesity and associated health problems. Thy1 (also called CD90), a widely used stem cell marker, blocks adipogenesis and reduces lipid accumulation. Thy1-knockout mice are prone to diet-induced obesity. Although the importance of Thy1 in adipogenesis and obesity is now evident, how its expression is regulated is not. We hypothesized that DNA methylation has a role in promoting adipogenesis and affects Thy1 expression. Using the methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-dC), we investigated whether DNA methylation alters Thy1 expression during adipogenesis in both mouse 3T3-L1 preadipocytes and mouse mesenchymal stem cells. Thy1 protein and mRNA levels were decreased dramatically during adipogenesis. However, 5-aza-dC treatment prevented that phenomenon. Methylation-sensitive pyrosequencing analysis showed that CpG sites at the Thy1 locus have increased methylation during adipogenesis, as well as increased methylation in adipose tissue from diet-induced obese mice. These new findings highlight the potential role of Thy1 and DNA methylation in adipogenesis and obesity.-Flores, E. M., Woeller, C. F., Falsetta, M. L., Susiarjo, M., Phipps, R. P. Thy1 (CD90) expression is regulated by DNA methylation during adipogenesis.

Vitamin A administration at birth promotes calf growth and intramuscular fat development in Angus beef cattle

BackgroundMarbling, or intramuscular fat, is an important factor contributing to the palatability of beef. Vitamin A, through its active metabolite, retinoic acid, promotes the formation of new fat cells (adipogenesis). As intramuscular adipogenesis is active during the neonatal stage, we hypothesized that vitamin A administration during the neonatal stage would enhance intramuscular adipogenesis and marbling.MethodsAngus steer calves (n = 30), in a completely randomized design, were randomly allotted to three treatment groups at birth, receiving 0, 150,000, or 300,000 IU of vitamin A at both birth and one month of age. A biopsy of the biceps femoris muscle was collected at two months of age. After weaning at 210 d of age, steers were fed a backgrounding diet in a feedlot until 308 d of age, when they were transitioned to a high concentrate finishing diet and implanted with trenbolone/estradiol/tylosin mixture. Steers were harvested at an average of 438 d of age. All diets were formulated to meet nutrient requirements.ResultsWeaning weight and weight during the backgrounding phase were linearly increased (P < 0.05) by vitamin A level, though no difference in body weight was observed at harvest. Intramuscular fat of steers at 308 d of age, measured by ultrasound, quadratically increased (P < 0.05) with vitamin A level from 4.0±0.26 % to 4.9±0.26 %. Similarly, carcass marbling score in the ribeye quadratically increased (P < 0.05).ConclusionAdministration of vitamin A at birth increased weaning weight and enhanced marbling fat development. Thus, vitamin A administration provides a practical method for increasing marbling and early growth of beef cattle.

The brominated flame retardant tetrabromobisphenol‐A increases DNA methylation at the THY1 (CD90) locus to promote adipogenesis

Obesity has been classically linked to poor diet/excessive calorie intake and insufficient physical activity. However, an emerging concept is that environmental pollutants may be driving the global obesity epidemic. The rapid increase in the prevalence of obesity in industrialized, developed and even undeveloped countries cannot be strictly accounted for by poor diet and physical inactivity. Environmental chemicals, termed “obesogens” can promote adipogenesis (fat cell formation). Tetrabromobisphenol‐A (TBBPA), a brominated flame retardant found in infant mattresses and electronics such as cell phones, is an obesogens. However, its mechanism of action remains unknown. We hypothesize that TBBPA promotes adipogenesis by decreasing levels of THY1 (CD90), a cell surface protein present on pre‐adipocytes, certain fibroblasts, and stem cells. We previously determined that fibroblasts are heterogeneous for THY1 expression, where only THY1‐/low fibroblasts differentiate into adipocytes, pointing to THY1's crucial role during adipogenesis and cell fate. Using the well‐established mouse pre‐adipocyte cell line (3T3‐L1), we determined that TBBPA reduces THY1 mRNA and protein levels, promoting adipogenesis. Epigenetic changes, such as increases in global DNA methylation are known to occur during adipogenesis and obesity. DNA hypermethylation typically silences gene expression. Therefore, we hypothesized that obesogens, such as TBBPA, alter epigenetic regulation of THY1 to decrease its expression, thereby priming precursor cells to become adipocytes. Using pyrosequencing, we found that CG rich regions on THY1 are hypermethylated during adipogenesis, resulting in decreased THY1 expression and cell differentiation to adipocytes. Using the methylation inhibitor, 5‐aza‐dC, we determined that the adipogenic effects of TBBPA are blunted when methylation is impeded, which results in increased THY1 levels. Our results confirm THY1 plays a critical role in adipogenesis and that its expression is regulated by increases in DNA methylation. Furthermore, TBBPA, a widely‐used flame retardant, increases DNA methylation at the Thy1 locus to promote adipogenesis. Environmental obesogens contribute to the worldwide obesity epidemic and their further study is critical to combating this epidemic.Support or Funding InformationP30 ES 001247, F31 ES027767‐02This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

CHARACTERISTICS OF UKRAINIAN GREY CATTLE BY DNA-MARKERS

CHARACTERISTICS OF UKRAINIAN GREY CATTLE BY DNA-MARKERS

Hormonal Regulation of Adipogenesis.

Adipose tissue includes multiple anatomical depots that serve as an energy reserve that can expand or contract to maintain metabolic homeostasis. During normal growth and in response to overnutrition, adipose tissue expands by increasing the volume of preexisting adipocytes (hypertrophy) and/or by generating new adipocytes (hyperplasia) via recruitment and differentiation of adipose progenitors. This so-called healthy expansion through hyperplasia is thought to be beneficial in that it protects against obesity associated metabolic disorders by allowing for the "safe" storage of excess energy. Remodeling adipose tissue to replace dysfunctional adipocytes that accumulate with obesity and age also requires new fat cell formation and is necessary to maintain metabolic health. Adipogenesis is the process by which adipose progenitors become committed to an adipogenic lineage and differentiate into mature adipocytes. This transition is regulated by complex array of transcriptional factors and numerous autocrine, paracrine, and endocrine signals. We will focus on hormonal factors that regulate adipocyte differentiation and their molecular mechanisms of actions on adipogenesis as studied in vitro and in vivo. Accumulating evidence indicates that adipose progenitors isolated from different adipose tissues exhibit intrinsic differences in adipogenic potential that may contribute to the depot and sex differences in adipose expansion and remodeling capacity. We will put special emphasis on the hormonal factors that are known to depot-dependently affect body fat accumulation and adipocyte development. © 2017 American Physiological Society. Compr Physiol 7:1151-1195, 2017.

Neprilysin facilitates adipogenesis through potentiation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway.

Neprilysin (NEP) is a zinc metallopeptidase that cleaves a number of small peptides into inactive forms. Despite the recent evidence of a significant correlation between the levels of NEP in plasma and the severity of obesity in humans, a cause-and-effect relationship or a functional role of NEP in obesity has remained uncertain. In this study, we show that NEP has a positive regulatory effect on fat cell formation from precursor cells. NEP increases the accumulation of cytoplasmic triglycerides in 3T3-L1 preadipocytes or the C3H10T1/2 mesenchymal stem cell line in differentiation conditions. Consistently, cells expressing NEP showed an increase in mRNA expression of adipogenic transcription factors, peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), and the adipocyte markers aP2 and adipsin. Furthermore, this NEP-enhanced induction of adipogenesis was found to require the enzymatic activity of NEP, leading to augmentation of the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signaling pathway. In summary, our results indicate that NEP accelerates adipogenesis through enhancement of insulin-mediated PI3K-Akt activation and imply a high therapeutic value of NEP in treating obesity and obesity-related disorders.

MicroRNA Regulatory Networks as Biomarkers in Obesity: The Emerging Role.

Even though it is a pandemic health problem worldwide, the pathogenesis of obesity is poorly understood. Recently, emerging studies verified that microRNAs (miRNAs) are involved in complicated metabolic processes including adipocyte differentiation, fat cell formation (adipogenesis), obesity-related insulin resistance and inflammation. Many regulatory networks have been identified in murine adipose tissue, but those in human adipose tissue are not as well known. In addition, miRNAs have been detected in circulation, and thus may be usable as diagnostic indicators. MiRNAs may play an important part in regulating metabolic functions in adipose tissues and, by extension, obesity and its associated disorders. Consequently, they may be potential candidates for therapeutic targets and biomarkers.

Extracts of common pulses demonstrate potent in vitro anti‐adipogenic properties

SummaryPulses are an important food source in many countries and also widely used as feed for livestock. Discovery of novel health benefits in pulses may contribute to improved diet and potential added value to crops. In this study, we examined the ability of extracts from faba bean, field pea and chickpea to inhibit the formation of fat droplets in an in vitro cell culture system that mimics the process of fat cell formation or adipogenesis. Both seed and hull extracts of all three pulses showed an inhibition of adipogenesis and the hull fraction and also contained higher levels of polyphenols compared with the seed extracts. At the molecular level, adipogenic inhibition was associated with a marked reduction in peroxisome proliferator‐activated receptor gamma (PPARG) gene expression. Furthermore, the field pea pulse extract was shown to inhibit pancreatic lipase activity at a similar level to the drug ‘orlistat’, which is commonly used to treat obesity.

Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytes.

Urolithins (Uro) are ellagic acid (EA)-derived metabolites produced by gut microbes. There is a growing interest in the biological activities of Uro. Our aim was to evaluate the impacts of Uro on regulating triglyceride (TG) accumulation using cultures of primary human adipocytes and hepatoma Huh7 cells. UroA, UroB, UroC, UroD, and iso-UroA were used to determine the effect of Uro on adipogenesis and lipogenesis. Individual Uro (30 μM) were added to human adipogenic stem cells during differentiation. UroA, UroC, and UroD, but not iso-UroA and UroB, significantly inhibited new fat cell formation by decreasing TG accumulation and adipogenic protein and gene expressions. The regulation of TG synthesis by Uro was investigated via metabolic chasing with radiolabeled precursors. UroA, UroC, and UroD attenuated TG accumulation, while increasing the fatty acid (FA) oxidation in adipocytes and h/epatoma Huh7 cells. Furthermore, UroC, UroD, and UroA promoted the phosphorylation of AMP-activated protein kinase, suggesting that Uro may alter energy-sensing metabolic pathways in primary human adipocytes. Taken together, our results demonstrated that UroA, UroC, and UroD, but not isoUroA and UroB, reduce TG accumulation and increase FA oxidation in adipocytes as well as hepatocytes.

Lentinan depresses 3T3-L1 fat cell formation by inhibiting PPARγ/AKT signaling pathway.

We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARγ activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARγ and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARγ mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARγ mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARγ mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARγ/AKT signaling pathway.