Acquired segmental sigmoid hypoganglionosis: A case report.

RATIONALE: Intestinal hypoganglionosis most commonly presents in infancy or childhood, with only a few cases reported in adults. Those are mainly diagnosed after elective surgery for long-standing constipation and megacolon. PATIENT CONCERNS: We report a case of a 48-year-old female from China who presented with symptoms of discontinuation of bowel movements for 2 months. A hard, round mass could be felt in her right lower abdomen. DIAGNOSIS: The following examination methods diagnosed acquired segmental sigmoid hypoganglionosis. An abdominal computed tomography revealed a dilatation of the colon and suspicious wall thickening of the sigmoid colon. Anorectal manometry revealed relaxation of the anal sphincter. Histological examination revealed lower numbers and the degeneration of ganglion cells. INTERVENTIONS: Sigmoidectomy and transverse colostomy. OUTCOMES: The patient recovered well from surgery. Three months after the surgery, barium enema revealed a recovery in colorectal dilatation. LESSONS: This case could help raise awareness of acquired segmental hypoganglionosis. Resection of TZ and enterostomy presents an effective remission strategy for patients at risk of anastomotic leakage due to poor intestinal conditions.

Increased cancer-specific mortality of very small size in carcinoembryonic antigen-elevated rectal cancer.

BACKGROUND: The present study aimed to investigate the cause-specific survival (CSS) of very small rectal cancer in the context of preoperative serum carcinoembryonic antigen (CEA) elevation. METHODS: Patients diagnosed with node-negative rectal cancer from the Surveillance, Epidemiology, and End Results (SEER) database from January 2004 to December 2010 meeting the inclusion criteria were identified for this study. The Cox proportional hazards regression analyses were conducted to identify independent factors associated with CSS. Pearson's chi-squared tests and Kaplan-Meier methods were performed. RESULTS: A total of 8,413 patients were included into our study. Kaplan-Meier analyses showed lower 7-year CSS rate of very small tumors (≤5 mm) compared to those larger than 40 mm (70.4% vs. 76.0%, log-rank P=0.469). Multivariate Cox analyses showed that patients with very small tumor size (≤5 mm) was also associated with a significantly increased risk of cancer-specific mortality compared with those with large tumor size (HR =2.567, 95% CI: 1.285 to 5.130, P=0.008, using ≥41 mm, C+ as a reference). CONCLUSIONS: Very small tumor size in the context of preoperative serum CEA elevation could be a surrogate for biological aggressiveness. Our finding would provide a better understanding of tumor biology for us and elicit more future biological researches.

The inhibitory effect of oridonin on colon cancer was mediated by deactivation of TGF-ß1/Smads-PAI-1 signaling pathway in vitro and vivo.

BACKGROUND: Oridonin, the main active component of Rabdosia rubescens, has been demonstrated to have anti-tumor effect on all kinds of cancer cells through various mechanisms and it has shown antitumor activity in some tumors partially via the suppression of TGF-ß/Smads signaling pathway. The aim of this study was to explore the anticancer effect of oridonin on human colon carcinoma and underlying mechanism in vitro and vivo. METHODS: CCK-8 assay was employed to assess cell viability. The key target genes and proteins involved in TGF-ß/Smads pathway was detected by RT-PCR, Western blotting and immunohistochemistry. The orthotopic transplantation tumor model of colon cance LOVO cell was introduced to detect anti-cancer effects in vivo. RESULTS: Oridonin inhibited the proliferation of colon cancer LOVO cells in a concentration and time dependent manner. In addition, oridonin reduced the levels of Smad2, Smad3, Smad4, PAI-1 and the phosphorylation of Smad2 and Smad3 induced by TGF-ß1 in vitro. Subsequently, we established an orthotopically implanted tumor model in nude mice and found that oridonin treatment significantly suppressed tumor growth, and which was accompanied by the down-regulation of Smad2, Smad3, Smad4, PAI-1 and p-Smad2, p-Smad3 expression levels. CONCLUSION: Our present study demonstrated that the growth inhibition of colon cancer by oridonin could be partially mediated through discontinuing TGF-ß1/Smads-PAI-1 signaling pathway, suggesting it as a promising agent in treating colorectal cancer.

Preoperative serum carcinoembryonic antigen elevation in stage I colon cancer: improved risk of mortality in stage T1 than in stage T2.

PURPOSE: This study aimed to investigate the implications of preoperative serum carcinoembryonic antigen (CEA) elevation in cause-specific survival (CSS) of patients diagnosed with stage I (T1N0M0 and T2N0M0) colon cancer. METHODS: Eligible patients diagnosed with stage I colon cancer from the Surveillance, Epidemiology, and End Results (SEER) database from January 2004 to December 2010 were included in this respective and propensity score-matched (PSM) study. Some Cox proportional hazards models were constructed to identify prognostic factors associated with oncologic outcomes of colon cancer. Pearson's chi-squared tests and Kaplan-Meier methods were performed. RESULTS: The median follow-up time of the whole cohort was 79 months. A total of 16,659 patients diagnosed with stage I colon cancer were identified from the SEER database. Multivariate Cox analyses showed that stage T1N0M0 in the context of serum CEA elevation (T1, CEA+) presented up to 158.4% increased risk of colon cancer-specific mortality compared with stage T1N0M0 in the context of normal serum CEA [hazard ratio (HR) = 2.584, 95% confidence interval (CI) = 2.167-3.082, P < 0.001]. After PSM, Kaplan-Meier survival curves of stage T1N0M0 colon cancer showed that 5-year CSS rates of normal and elevated CEA were 94.8% and 96.6% (P < 0.001). CONCLUSIONS: This large population-based and propensity score-matched study with long follow-up time provides the first evidence that stage T1N0M0 colon cancer with the elevation of preoperative serum CEA would be a surrogate of aggressive tumor biology and predict poor prognosis. In addition, this subgroup of colon cancer might need to be paid more attention of clinicians.

Wnt/ß-catenin signaling pathway is involved in induction of apoptosis by oridonin in colon cancer COLO205 cells.

BACKGROUND: Oridonin has been demonstrated to have anticancer effect on all kinds of cancer cells and it has shown anti-tumor activity in some tumors partially via the inactivation of Wnt/ß-catenin signaling pathway. The study investigated the anticancer effect of oridonin on colon carcinoma cell line COLO205 and explored underlying mechanism. METHODS: Cell Counting Kit-8 (CCK-8) assay was performed to assess cell viability. Flow cytometry was performed to analyze the apoptosis. The key target genes and proteins involved in Wnt/ß-catenin pathway were detected by quantitative polymerase chain reaction (qPCR) and Western blotting. The xenograft tumor model of colon cancer COLO205 cell was introduced to detect anti-tumor effects in vivo. Transferase-mediated dUTP nick end labeling (TUNEL) assay was adopted to test the apoptotic cells in the tumor tissues. RESULTS: Oridonin inhibited the proliferation of colon cancer COLO205 cells in a dose-dependent and time-dependent manner. Oridonin induced apoptosis by increasing the cleavage of caspases in vitro. Furthermore, the expression levels of ß-catenin and its downstream targets, including c-myc, cyclinD1 and survivin were significantly reduced. Nevertheless the knockdown of ß-catenin by specific small interfering RNA (siRNA) could augment the anti-proliferative and pro-apoptotic effects by oridonin in COLO205 cells. Meanwhile, oridonin also increased protein expression level of glycogen synthase kinase 3ß (GSK3ß) and decreased the phosphorylation level of GSK3ß. In vivo, oridonin treatment significantly suppressed tumor growth of COLO205 cell xenografts, and which was accompanied by the restrain of Wnt/ß-catenin pathway. CONCLUSIONS: Our present study demonstrated that the growth inhibition and apoptosis induction in colon cancer COLO205 cells by oridonin could be partially mediated through discontinuing Wnt/ß-catenin signaling pathway.

Prognostic accuracy of different lymph node staging systems in rectal adenocarcinoma with or without preoperative radiation therapy.

BACKGROUND AND OBJECTIVE: A variety of different lymph node (LN) staging systems have been developed to describe the lymph node status accurately. We aim to compare the prognostic accuracy of American Joint Committee on Cancer seventh N stage relative to negative number of lymph node (nLN), lymph node ratio (LNR) and log odds of metastatic lymph nodes (LODDS) in rectal adenocarcinoma (RC). METHODS: A total of 19 167 Stage II-III rectal cancer patients who underwent surgical resection of rectal adenocarcinoma were identified from Surveillance, Epidemiology and End Results database. Akaike's Information Criterion (AIC) and the Harrell's concordance index (c statistic) were used to evaluate the relative discriminative power of the different LN staging systems. RESULTS: Of the 19 167 patients, 10 958 received preoperative radiotherapy (pre-RT cohort) and 8209 patients were treated with surgical resection directly (SURG cohort). When assessed using categorical cutoff values, LNR has a somewhat better prognostic accuracy both in pre-RT (c-index: 0.62; AIC: 2988.6) and SURG groups (c-index: 0.60; AIC: 3359.8). Further analysis based on different total number of lymph node (TNLN) suggested that when less than 10 lymph nodes were retrieved, LNR exhibited significant superiority (pre-RT: c-index: 0.597, AIC: 1006.8; SURG: c-index: 0.560, AIC: 810.5). When analyzed as a continuous variable, the LODDS system performed the best and was not impacted by TNLN. CONCLUSION: When assessed as a categorical variable, LNR was the most powerful method to predict survival for Stage II-III RC patients with limited TNLN. Rather, LODDS was the most accurate staging system regardless of the TNLN when LN status was modeled as continuous variable.

A Modified Preauricular Approach for Treating Intracapsular Condylar Fractures to Prevent Facial Nerve Injury: The Supratemporalis Approach.

PURPOSE: The facial nerve remains at risk of injury with the preauricular approach; thus, preservation of the functional integrity of the facial nerve is considered an important factor in the success of temporomandibular joint surgery. The aim of this study was to prevent facial nerve injury using the supratemporalis approach in the treatment of intracapsular condylar fractures. MATERIALS AND METHODS: In this prospective cohort study, the population consisted of patients diagnosed with intracapsular condylar fractures who received surgical treatment from July 2005 to May 2014. Patients in the experimental group were treated with the supratemporalis approach, and patients in the control group were treated with the traditional preauricular surgical technique. The primary outcome variable was facial never injury. The continuity correction χ(2) and test Student t test were used. RESULTS: Eighty-four patients (112 sides) with intracapsular condylar fractures were treated surgically (56 men, 28 women; mean age, 29.85 yr; range, 4 to 70 yr); 44 patients (64 sides) were treated with the supratemporalis approach and 40 patients (48 sides) were treated with the traditional preauricular approach. Facial contours and functions recovered well postoperatively in all 84 patients. Seven cases of facial nerve injury, 2 of which were permanent, were observed in the group treated with the traditional preauricular approach, and no facial nerve injuries were observed in the group treated with the supratemporalis approach. None of the patients sustained auriculotemporal syndrome or wound infection complications. CONCLUSIONS: The supratemporalis approach prevented facial nerve injury and did not increase the frequency of other complications.

Human Umbilical Cord Mesenchymal Stem Cells: A New Therapeutic Option for Tooth Regeneration.

Tooth regeneration is considered to be an optimistic approach to replace current treatments for tooth loss. It is important to determine the most suitable seed cells for tooth regeneration. Recently, human umbilical cord mesenchymal stem cells (hUCMSCs) have been regarded as a promising candidate for tissue regeneration. However, it has not been reported whether hUCMSCs can be employed in tooth regeneration. Here, we report that hUCMSCs can be induced into odontoblast-like cells in vitro and in vivo. Induced hUCMSCs expressed dentin-related proteins including dentin sialoprotein (DSP) and dentin matrix protein-1 (DMP-1), and their gene expression levels were similar to those in native pulp tissue cells. Moreover, DSP- and DMP-1-positive calcifications were observed after implantation of hUCMSCs in vivo. These findings reveal that hUCMSCs have an odontogenic differentiation potency to differentiate to odontoblast-like cells with characteristic deposition of dentin-like matrix in vivo. This study clearly demonstrates hUCMSCs as an alternative therapeutic cell source for tooth regeneration.

Expression of miR-221 in colon cancer correlates with prognosis.

MicroRNAs are increasingly important in the study of cancer because of their ability to down regulate the expression of tumor suppressors and promote tumorigenesis. Here, miR-221, which is dysregulated in various tumors, was investigated for its expression in colon cancer tissues and its correlation with patient prognosis. Colon cancer tissue samples were obtained from 182 individuals who underwent surgical resection in our hospital from June 2008 to September 2009. Real-time PCR was used to detect the expression of miR-221 in these tissues. Patient survival was determined by telephone interview, and survival curves were plotted by using the Kaplan-Meier method and compared by the Log-rank test. Statistical methods also included X(2) test and Cox proportional hazard regression model. Differences in the expression of miR-221 by gender, pathology, and pathological staging were not statistically significant (P>0.05), but differences in the expression of miR-221 among age groups were statistically significant (P<0.05). A survival analysis indicated that high expression of miR-221 was closely associated with a shorter survival time (P<0.05). Further, later p-TNM (hazard ratio, HR=2.973, 95% confidence interval, CI: 1.329-6.519, P=0.003) and high expression of miR-211 (HR=2.394, 95% CI: 1.210-4.910, P=0.006) were identified as risk factors for colon cancer prognosis. Thus, high miRNA-221 expression might be a prognostic marker of colon cancer patients. The high expression of miRNA-221 was associated with poor prognosis of patients with colon cancer.

Bone marrow-derived stromal cells are more beneficial cell sources for tooth regeneration compared with adipose-derived stromal cells.

Tooth loss is presently a global epidemic and tooth regeneration is thought to be a feasible and ideal treatment approach. Choice of cell source is a primary concern in tooth regeneration. In this study, the odontogenic differentiation potential of two non-dental-derived stem cells, adipose-derived stromal cells (ADSCs) and bone marrow-derived stromal cells (BMSCs), were evaluated both in vitro and in vivo. ADSCs and BMSCs were induced in vitro in the presence of tooth germ cell-conditioned medium (TGC-CM) prior to implantation into the omentum majus of rats, in combination with inactivated dentin matrix (IDM). Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the mRNA expression levels of odontogenic-related genes. Immunofluorescence and immunohistochemical assays were used to detect the protein levels of odontogenic-specific genes, such as DSP and DMP-1 both in vitro and in vivo. The results suggest that both ADSCs and BMSCs have odontogenic differentiation potential. However, the odontogenic potential of BMSCs was greater compared with ADSCs, showing that BMSCs are a more appropriate cell source for tooth regeneration.

MiR-540 as a novel adipogenic inhibitor impairs adipogenesis via suppression of PPARγ.

A better understanding of the molecular mechanisms in adipogenesis may provide new insights into adipose tissue-related diseases. Recently, microRNAs (miRNAs) have emerged as a class of epigenetic regulators of stem cell differentiation. In this study, we found that miR-540 was an essential negative regulator of adipogenic differentiation in adipose tissue-derived stromal cells (ADSCs). Lentivirus-mediated overexpression of miR-540 resulted in blockade of the expression of C/EBP-α and PPARγ, the two master transcription factors of adipogenesis, and deficient lipid accumulation, whereas inhibition of miR-540 promoted these processes. Target gene reporter assays showed that miR-540 directly targeted the 3'-untranslated region (3'UTR) of PPARγ, resulting in a decrease of PPARγ protein expression. Collectively, these data suggest that miR-540 represents a new adipogenic inhibitor by, at least in part, targeting PPARγ.

A novel electrochemical method to determine α-amylase activity.

In this paper, we report a novel electrochemical method that can be developed as a biosensor for simple and direct determination of α-amylase activity. The method is based on the hydrolysis of maltopentaose, the substrate of the enzyme, which is immobilized on the surface of a gold electrode, and the induced charge changes of the substrate-modified electrode. Specifically, the substrate maltopentaose is immobilized onto a gold electrode surface via a simple and direct immobilization technique that involves a one-step and site-specific attachment of unmodified maltopentaose to the hydrazide-derivatized surface. So, by analyzing the electrochemical signal obtained from the electro-active molecule [Ru(NH3)5Cl](2+) during the hydrolysis of maltopentaose, the determination of α-amylase activity is achieved. Under optimized conditions, α-amylase activity can be assayed with a detection limit of 0.022 U mL(-1). The biosensor exhibits a rapid response, good stability and anti-interference ability. Furthermore, the biosensor has also been successfully applied to detect α-amylase in human serum, which shows acceptable accuracy compared to the currently used clinical method. The proposed method in this work may also have potential application of α-amylase determination in real blood samples, diagnostics and food production in the future.

Surgical planning, three-dimensional model surgery and preshaped implants in treatment of bilateral craniomaxillofacial post-traumatic deformities.

PURPOSE: The purpose of the present study was to explore the treatment and outcomes of bilateral craniomaxillofacial post-traumatic deformities with surgical planning, 3-dimensional (3D) model surgery, and preshaped implants. MATERIALS AND METHODS: We analyzed the preoperative computed tomography (CT) data and designed preliminary surgical plans for 3 patients with bilateral craniomaxillofacial post-traumatic deformities. 3D resin skull models were produced using rapid prototyping technology, and 3D model surgery was performed to determine the location, reduction direction, and shift distance of the osteotomy and to optimize the surgical plans. Titanium plates or mesh were preshaped on the models and then implanted into the patients. The complications, symmetry of the maxillofacial regions, mouth opening, and occlusion were observed 1 month postoperatively. RESULTS: The patients had good recovery of their facial contour, occlusion, and mouth opening and acceptable symmetry of the bilateral maxillofacial regions. No complications were observed. CONCLUSIONS: The combination of surgical planning, 3D model surgery, and preshaped implants can provide surgical accuracy and efficiency and good therapeutic outcomes in the treatment of bilateral craniomaxillofacial post-traumatic deformities.

The combination of atomic force microscopy and sugar analysis to evaluate alkali-soluble Canna edulis Ker pectin.

Alkali-soluble pectin, which has been extracted from Canna edulis Ker, was characterized by single sugar determination and atomic force microscopy (AFM). The results indicated that the amounts of four predominant sugars including arabinose (Ara), glucose (Glc), galactose (Gal) and galacturonic acid (GalA) significantly decreased during the process of mild acid hydrolysis. The decreasing rates of these four sugars followed a sequential order of Ara>Gal>Glc>GalA. The homogalacturonan (HG) chain present in pectin, and the quantity of branched material is greater than the sample containing the main neutral sugars. The results indicated that the neutral sugar and HG side chains are attached to pectin as part of the rhamnogalacturonan I (RGI) complex. Moreover, hydrolysis leads to the reduction of mean lengths of backbone and branch, as well as the number/weight-average molecular weight. Meanwhile, the amount of short chain fractions increased during hydrolysis. Furthermore, the decrease of the polymerization degree of alkali-soluble C. edulis pectin as a function of the hydrolysis time could be described by a first-order exponential decay function.

MicroRNA-143 regulates adipogenesis by modulating the MAP2K5-ERK5 signaling.

A better understanding of the molecular mechanisms that regulate adipose tissue-derived stromal cell (ADSC) differentiation could provide new insight into some adipose-tissue-related disease. The differentiation of ADSCs into adipocytes is a complex physiological process that includes clonal expansion, growth arrest, and terminal differentiation. Here the role of microRNA-143 (miR-143) during ADSC adipogenic differentiation was systematically investigated. We found that miR-143 expression was transiently decreased after adipogenic induction while increased from day 3 and peaked on day 7 after induction. We show for the first time that the role of miR-143 is not consistent in the differentiation process. The regulatory role depends on the differentiation stage that miR-143 acts on. When miR-143 is overexpressed during the clonal expansion stage, the adipogenic differentiation of ADSCs is inhibited, whereas the overexpression of miR-143 during the growth arrest stage or terminal differentiation stage promotes differentiation. Further we firstly demonstrate that miR-143 plays the modulational role by directly repressing MAP2K5, a key member of the MAPKK family in the MAPK signaling pathway. These findings suggest that miR-143 plays an important role in adipose tissue formation, with special implications for some metabolic disease in which the amount and/or function of adipose tissue is altered.

A novel negative regulator of adipogenesis: microRNA-363.

The differentiation of adipose tissue-derived stromal cells (ADSCs) into adipocytes involves a highly orchestrated series of events that includes cell lineage commitment, mitotic clonal expansion, growth arrest, and terminal differentiation. However, the molecular mechanisms controlling adipogenesis are not yet completely understood. In this study, we investigated whether microRNAs (miRNAs) play a role in adipocyte differentiation. Microarray analysis was performed to determine the miRNA expression profile during ADSC differentiation, and miR-363 was found to be one of the most significantly downregulated miRNAs. We show that the overexpression of miR-363 in ADSCs inhibited mitotic clonal expansion and terminal differentiation. Furthermore, ectopic introduction of miR-363 into ADSCs markedly reduced the levels of E2F3, a key transcription factor that regulates growth and proliferation during mitotic clonal expansion. Finally, using an EGFP/RFP reporter assay, we demonstrate that miR-363 can directly target the 3'UTR of E2F3. Taken together, these results suggest that miR-363 regulates the transition from mitotic clonal expansion to terminal differentiation during adipogenesis in ADSCs, at least in part, by targeting E2F3.

Physicochemical property of starch-pectin conjugates with resistance to enzymatic activity.

BACKGROUND: In view of the high nutritional values and bioactivities of resistant starch and pectin, it would be a good choice to chemically combine pectin and starch to give a new type of chemically modified resistant starch. RESULT: A new type of chemically modified resistant starch has been prepared by cross-linking starch and pectin using sodium trimetaphosphate. Starch-pectin conjugates can well prevent the hydrolysis catalysed by different enzymes, such as α-amylase, amyloglucosidase, pancreatin as well as ß-amylase and glucosidase. Although the conjugates do not change the crystal type of starch, they increase the degree of crystallinity. Moreover, thermal stability and structural homogeneity of the conjugates are positively correlated with double-helical order in the crystalline region. CONCLUSION: This study gives a new method for the preparation of resistant starch-pectin conjugates which can be widely used as a new type of food additive in the industry.

Oridonin induces apoptosis in SW1990 pancreatic cancer cells via p53- and caspase-dependent induction of p38 MAPK.

Oridonin, an active component isolated from Rabdosia rubescens, has been reported to exhibit antitumor effects. In the present study, we evaluated the antitumor activity and the mechanisms of action of oridonin in pancreatic cancer. Oridonin treatment significantly induced apoptotic cell death in SW1990 pancreatic cancer cells in a dose-dependent manner. Additionally, cell apoptosis was markedly inhibited by PFT α (pifithrin α), a p53-specific inhibitor, which was applied to evaluate the function of p53, showing that p53 was responsible for the cytotoxity of oridonin. Moreover, oridonin increased the expression of p-p53 with a concomitant increase in p21 in the SW1990 cells. Following treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB203580 (p38 inhibitor), the cytotoxity of oridonin was not influenced by JNK (SP600125) and ERK (PD98059), but these effects were opposite to the cytotoxity of oridonin observed with SP203580 treatment. These findings confirmed that orodonin-induced apoptosis was p38-dependent, but JNK- and ERK-independent. Furthermore, the activation of the p38 kinase promoted the activation of p53 and its downstream target p21, and further caused caspase-9 and -3 activation, as demonstrated by evidence showing that the p38 inhibitor SB203580 not only blocked the phosphorylation of p38 but also reduced the activation of p53, p21 and caspase-9 and -3. Collectively, these results suggest that p53-dependent and caspase-dependent induction of p38 MAPK directly participates in apoptosis induced by oridonin.

Activated effect of lignin on α-amylase.

This paper reports a new kind of activator of α-amylase, lignin, which can greatly increase α-amylase activity. The promoted ratio of lignin is even much higher than that of chloride ion, the traditional activator of α-amylase. Further experimental results reveal that lignin may interact with α-amylase to form a 1:1 complex with a binding constant of 4.47×10(5) M(-1). The binding is spontaneous and lignin/α-amylase complex formation is an exothermal reaction. Hydrogen bonding plays a key role and non-radiation energy transfers from α-amylase to lignin in the binding process. Lignin, combining with α-amylase, conforms to a first-order exponential decay function. The formation of the lignin/α-amylase complex results in the reduction of α-helical content from 57.7% to 53.9%, the increase of the polarity around tryptophan residues, the decrease of the hydrophobicity, and the enlargement of protein granule volume. This work will give a deeper insight into lignin as a kind of dietary fibre, known as an important food functional factor. Furthermore, it also contributes to the exploration of an activator of α-amylase, used in the food industry.

microRNAs regulate adipocyte differentiation.

The number of adipocytes is relevant to the extent of differentiation from pluripotent stem cells into pre-adipocytes, whereas the size of adipocytes relates to the extent of differentiation from pre-adipocytes into mature fat cells and the accumulation of triglyceride. Investigation of the molecular regulatory mechanism of adipocyte differentiation is not only essential for understanding the physiological processes of adipogenesis, but it is also important for identifying new biomarkers and therapeutic targets for some metabolic diseases, such as obesity and diabetes. microRNAs (miRNAs) appear to play important roles in adipocyte differentiation. During adipogenesis, miRNAs can accelerate or inhibit adipocyte differentiation by acting on transcription factors, regulating signalling pathways related to adipogenesis, or blocking the mitotic clonal expansion stage, thus regulating adipocyte development. The regulatory role of some miRNAs varies in different species or different cells. In this review, the biological characteristics of miRNA and the adipocyte differentiation process are concisely discussed. Recent advances in our understanding of the role of miRNAs in adipocytes development or adipogenesis are discussed.