Impact of pre-existing frailty on survival outcomes in solid-organ transplant candidates and recipients: A meta-analysis.

BACKGROUND: There is controversy surrounding the association between preexisting frailty and increased mortality in candidates and recipients of solid-organ transplants. This meta-analysis aimed to evaluate the impact of preexisting frailty on survival outcomes in solid-organ transplant candidates and recipients. METHODS: A systematic search was conducted in the PubMed, Web of Sciences, and Embase databases until October 2, 2023. Two reviewers independently selected the eligible studies according to the PECOS criteria: Participants (candidates and recipients of solid-organ transplants), Exposure (frailty), Comparison (no-frailty), Outcomes (waitlist or posttransplant mortality), and Study design (retrospective or prospective cohort studies). The pooled effects were summarized by pooling the adjusted hazard ratio (HR) with 95 % confidence intervals (CI) for the frail patients than those without frailty. RESULTS: Sixteen studies with 10091 patients met the eligibility criteria. Depending on the frailty tools used, the prevalence of frailty in solid-organ transplant candidates/recipients ranged from 4.6 % to 45.1 %. Frailty was significantly associated with an increased risk of waitlist mortality (HR 2.44; 95 % CI 1.84-3.24) and posttransplant mortality (HR 2.23; 95 % CI 1.61-3.09) in solid-organ transplant candidates and recipients, respectively. Subgroup analyses showed that the association of preexisting frailty with waitlist mortality and posttransplant mortality appeared to stronger in kidney transplant candidates (HR 2.70; 95 % CI 1.93-3.78) and lung transplantation recipients (HR 2.52; 95 % CI 1.23-5.15). CONCLUSION: Frailty is a significant predictor of reduced survival in solid-organ transplant candidates and recipients. Assessment of frailty has the potential to identify patients who are suitable for transplantation.

Sarcopenia defined by the psoas muscle mass or quality is associated with poor survival in patients with aortic aneurysm undergoing surgery: A meta-analysis.

BACKGROUND: The impact of sarcopenia estimated by the skeletal muscle mass or quality on survival remains controversial in patients with aortic aneurysm. This meta-analysis aimed to assess the association between sarcopenia defined by the psoas muscle mass or quality and all-cause mortality in patients with aortic aneurysm. METHODS: We comprehensively searched PubMed, Web of Science, and Embase databases until December 31, 2022. Studies investigating the association of CT-derived psoas muscle mass (psoas muscle area [PSA] and psoas muscle index [PMI]) or quality (lean PSA [LPSA]) with all-cause mortality in patients with aortic aneurysm undergoing surgery were included. RESULTS: Eighteen studies reporting on 19 articles, enrolling 4767 patients were identified. A comparison of the bottom with the top psoas muscle mass, the pooled adjusted hazard ratios (HR) of all-cause mortality was 2.34 (95% confidence intervals [CI] 1.58-3.47). Low psoas muscle mass was associated with an increased risk of all-cause mortality when defined by the PSA (HR 2.01; 95% CI 1.42-2.75) or PMI (HR 2.37; 95% CI 1.24-4.55). Per 1 cm2 PMA increase conferred a 10% reduction in all-cause mortality. Patients with bottom LPMA had an increased risk of all-cause mortality (HR 3.27; 95% CI 1.90-5.60). Each 100 cm2 × HU LPMA increase conferred a 15% reduction in all-cause mortality. CONCLUSIONS: Sarcopenia defined by the low psoas muscle mass or quality independently predicts all-cause mortality in patients with aortic aneurysm. However, the overall certainty of evidence for the categorical analysis of psoas muscle mass was downgraded by the presence of publication bias and significant heterogeneity.

Abrogation of ARF6 in promoting erastin-induced ferroptosis and mitigating capecitabine resistance in gastric cancer cells.

Background: ADP ribosylation factor 6 (ARF6) is a member of the Rat sarcoma virus (RAS) superfamily that is involved in the regulation of vesicular trafficking, membrane lipid remodeling, and signaling pathways. Our earlier work discovered that ARF6, as a downstream effector of the Kirsten rat sarcoma viral oncogene (Kras)/extracellular signal-regulated kinases (ERK) signaling pathway, may increase proliferation and induce the Warburg effect in gastric cancer (GC) cells. Additionally, ARF6 appears to be a potential biomarker for predicting the prognosis of GC. Ferroptosis has recently been described as a type of nonapoptotic iron-dependent cell death that is strongly associated with the Kras mutation. Therefore, it is critical to continue investigating the link between ARF6 and ferroptosis. Methods: We first created ARF6 silenced cancer cell lines with lentivirus transfection. The knockdown efficiency was confirmed through quantitative polymerase chain reaction (qPCR) and western blotting. Subsequently, we used Cell Counting Kit-8 (CCK-8) and malondialdehyde (MDA) assay for lipid peroxidation measurement. Following this, qPCR and western blotting were conducted to clarify the mechanism involved. Finally, immunohistochemistry was used to stain human GC samples. Results: Our findings established that, whereas ARF6 did not directly regulate lipid peroxidation, it did render GC cells susceptible to oxidative stress, particularly erastin-induced lipid peroxidation. Additionally, our research demonstrated that ARF6 may control capecitabine resistance via several routes. Conclusions: ARF6 may play a critical role in the development of GC.

Clinical significance of expression of fibrous sheath interacting protein 1 in colon cancer.

BACKGROUND: The occurrence and development of colon cancer are complex, involving a variety of genetic changes, such as mutation and activation of oncogenes, inactivation of tumour suppressor genes, and aberrant proliferation and apoptosis regulation mechanisms. Fibrous sheath interacting protein 1 (FSIP1) is a newly discovered oncogene that is frequently activated in a variety of tumours such as breast cancer and bladder cancer. However, the clinical significance of FSIP1 in colon cancer is unclear. In this study, we analysed the clinical significance of expression of FSIP1 in human colon cancer, aimed to clarify the biological role of FSIP1 in the development and progression of colon cancer. AIM: To investigate the clinical significance of expression of FSIP1 in colon cancer. METHODS: From March 2011 to March 2014, 302 specimens of tumour tissues and paracancerous tissues were obtained from patients pathologically diagnosed with colon cancer at Shengjing Hospital of China Medical University. Immunohistochemistry was used to detect FSIP1 expression in colon cancer tissues and adjacent normal tissues. Spearman correlation coefficient and Cox regression analyses were used to determine the relationship between FSIP1 expression and clinicopathological factors and prognosis, as well as the impact on survival. RESULTS: Compared with its expression in adjacent normal tissues, FSIP1 was expressed at higher levels in colon cancer tissues. Spearman correlation analysis showed that high expression of FSIP1 was positively correlated with clinicopathological stage, lymph node metastasis, and poor prognosis in colon cancer; it was negatively correlated with the degree of tumour differentiation. Cox regression analysis showed that high FSIP1 expression was an independent risk factor for the prognosis of colon cancer patients. CONCLUSION: High expression of FSIP1 may be one of the important factors affecting the clinical outcome of colon cancer patients and leading to poor prognosis.

Gastric Sleeve Surgery Alleviates Obesity-Associated Insulin Resistance and Suppresses Endoplasmic Reticulum Stress in Adipose Tissue of db/db Mice.

OBJECTIVE: The aims of this study were to evaluate the effects of gastric sleeve surgery on diabetes remission in db/db mice as well as to determine the underlying mechanisms. METHODS: Thirty spontaneously obese, diabetic mice (C57BL/Ksj-db/db) were randomly divided into three groups: sleeve gastrectomy group, sham-operated group, and control db/db group. Ten db/m lean mice were used as nondiabetic littermate controls. All mice were sacrificed on day 28. The fasting plasma glucose, serum insulin, lipid profile, and oral glucose tolerance were measured pre- and postoperatively. Inflammatory cytokines (TNF-α and IL-6), endoplasmic reticulum (ER) stress-related markers (GRP78, PERK, IRE-1, and ATF6), and glucose transporter 4 (GLUT4) in the adipose tissue were assayed. RESULTS: Sleeve gastrectomy significantly reduced the body weight and food intake in the db/db mice. This surgery improved glucose and lipid metabolism, as manifested by the decrease in the fasting plasma glucose level and partial restoration of lipid abnormalities. Also, the surgery improved glucose tolerance and alleviated insulin resistance in db/db mice. Sleeve gastrectomy surgery induced downregulation of the inflammatory adipocytokines TNF-α and IL-6; suppressed expression of the ER stress-related markers GRP78, PERK, IRE-1, and ATF-6; and increased the expression and distribution of GLUT4 in adipose tissue of db/db mice. CONCLUSION: The improvement in glucose tolerance following sleeve gastrectomy is associated with alleviation of insulin resistance, reduction of inflammatory adipocytokine levels, and suppression of ER stress. Further studies are needed to assess whether these effects have a causal role.

Safety and efficacy for robot-assisted versus open pancreaticoduodenectomy and distal pancreatectomy: A systematic review and meta-analysis.

BACKGROUND: This meta-analysis was conducted to compare the clinical safety and efficacy of robot-assisted pancreaticoduodenectomy (RAPD) or robot-assisted distal pancreatectomy (RADP) with open surgery. METHODS: Multiple databases (PubMed, Medline, EMBASE and Cochrane Library) were searched to identify studies comparing the outcomes of RAPD and open pancreaticoduodenectomy (OPD) or RADP and open distal pancreatectomy (ODP) (up to December 31, 2017). Fixed and random effects models were applied according to different conditions. RESULTS: Fifteen non-randomized controlled trials (11 RAPD vs. OPD and 4 RADP vs. ODP) involving 3690 patients were included. Robot-assisted surgery had longer operative time (RAPD vs. OPD: P = 0.0005; RADP vs. ODP: P < 0.00001) but lesser blood loss than open surgery (RAPD vs. OPD: P = 0.0009; RADP vs. ODP: P = 0.0007). RAPD was associated with less wound infection, a lower positive margin rate, lower overall complications, and faster postoperative off-bed activity. There was no significant difference in the lymph node yield, the rate of pancreatic fistula, delayed gastric emptying, reoperation, length of hospital stay and mortality between the two groups. Compared with ODP, RADP was associated with less blood transfusion, fewer lymph nodes harvested, lower complications and shorter hospital stay. There was no significant difference between the two groups in the rate of spleen preservation, positive margin, pancreatic fistula, and mortality. CONCLUSIONS: Robot-assisted surgery is a safe and feasible alternative to OPD and ODP with regard to perioperative outcomes. However, due to the lack of high-quality randomized controlled trials, the evidence is still limited.

Transcription factor ATF3 mediates the radioresistance of breast cancer.

This study was designed to research the influence of activating transcription factor 3 (ATF3) on the radioresistance of breast cancer. ATF3 expression was measured by qRT-PCR and immunohistochemistry. Cancerous cell lines were cultured in vitro, and the expression of ATF3 was gauged by both qRT-PCR and Western blot before and after the radiation therapy. Cellular cycle and apoptosis were analysed by flow cytometry. Changes in the expression of corresponding proteins in the downstream pathways were identified by Western blot. Tumour xenograft was used to evaluate the effect of ATF3 in vivo. ATF3 was observed stronger in breast cancer tissues and cells. After radiation therapy, the expression of ATF3 in breast cancer cells was up-regulated. Silencing ATF3 could promote G2/M phase block, facilitate cell apoptosis and decrease clonogenic survival rate. The overexpression of ATF3 could curb G2/M-phase block, cell apoptosis and increase clonogenic survival rate. Overexpression ATF3 could increase radioresistance by up-regulating the level of phosphorylation of Akt in the PI3K/Akt signalling pathway. Radioresistance of breast cancer cells could be alleviated by inhibiting the PI3K/Akt signalling pathway. ATF3 could also promote radioresistance in vivo. ATF3 gene was able to promote radioresistance of breast cancer cells.

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells.

BACKGROUND/AIMS: Next-generation sequencing (NGS) has revealed abundant long noncoding RNAs (lncRNAs) that have been characterized as critical components of cancer biology in humans. The present study aims to investigate the role of the lncRNA KCNQ1OT1 in breast cancer (BRCA) as well as the underlying molecular mechanisms and functions of KCNQ1OT1 involved in the progression of BRCA. METHODS: The Cancer Genome Atlas (TCGA) and StarBase v2.0 were used to obtain the required gene data. Dual luciferase reporter gene assays were conducted to verify the relevant intermolecular target relationships. QRT-PCR and Western blot were performed to measure the expression levels of different molecules. Cell proliferation was detected by using the MTT and colony formation assays, while cell migration and invasion were examined by transwell assay. Variations in cell apoptosis and cell cycle were determined through flow cytometry. A tumor xenograft model was applied to assess tumor growth in vivo. RESULTS: KCNQ1OT1 was found to be remarkably highly expressed in BRCA tissues and cells. KCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2. CONCLUSION: The KCNQ1OT1/miR-145/CCNE2 axis plays a critical regulatory role in BRCA, potentially giving rise to BRCA tumorigenesis and progression. These findings provide valuable evidence for improving the diagnosis and treatment of BRCA in the future.

LncRNA HOTAIR influences cell growth, migration, invasion, and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer.

To study the regulatory effect of lncRNA HOTAIR/miR-20a-5p/HMGA2 axis on breast cancer (BC) cell growth, cell mobility, invasiveness, and apoptosis. The microarray data of lncRNAs and mRNAs with differential expression in BC tissues were analyzed in the Cancer Genome Atlas (TCGA) database. LncRNA HOX transcript antisense RNA (lncRNA HOTAIR) expression in BC was assessed by qRT-PCR. Cell viability was confirmed using MTT and colony formation assay. Cell apoptosis was analyzed by TdT-mediated dUTP nick-end labeling (TUNEL) assay. Cell mobility and invasiveness were testified by transwell assay. RNA pull-down and dual luciferase assay were used for analysis of the correlation between lncRNA HOTAIR and miR-20a-5p, as well as relationship of miR-20a-5p with high mobility group AT-hook 2 (HMGA2). Tumor xenograft study was applied to confirm the correlation of lncRNA HOTAIR/miR-20a-5p/HMGA2 axis on BC development in vivo. The expression levels of the lncRNA HOTAIR were upregulated in BC tissues and cells. Knockdown lncRNA HOTAIR inhibited cell propagation and metastasis and facilitated cell apoptosis. MiR-20a-5p was a target of lncRNA HOTAIR and had a negative correlation with lncRNA HOTAIR. MiR-20a-5p overexpression in BC suppressed cell growth, mobility, and invasiveness and facilitated apoptosis. HMGA2 was a target of miR-20a-5p, which significantly induced carcinogenesis of BC. BC cells progression was mediated by lncRNA HOTAIR via affecting miR-20a-5p/HMGA2 in vivo. LncRNA HOTAIR affected cell growth, metastasis, and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer.

LncRNA PART1 modulates toll-like receptor pathways to influence cell proliferation and apoptosis in prostate cancer cells.

We investigated thoroughly the effect of lncRNA PART1 on prostate cancer cells proliferation and apoptosis, through regulating toll-like receptor (TLR) pathways. LncRNA PART1 expression was also examined by quantitative real-time polymerase chain reactions (qRT-PCR) in human tissues and the cells lines LNCaP and PC3. After transfection with si-PART1 or control constructs, the cell viability was measured by MTS and colony formation assays. In addition, the apoptosis rate of the prostate cancer cells was validated by TUNEL staining. Relationships between lncRNA PART1 expression and TLR pathway genes were demonstrated by qRT-PCR and Western blotting. High levels of lncRNA PART1 expression were correlated with advanced cancer stage and predication of poor survival. LncRNA PART1 levels was increased in PCa cells treated with 5α-dihydrotestosterone (DHT), confirming PART1 was directly induced by androgen. Moreover, down-regulation of lncRNA PART1 inhibited prostate cancer cell proliferation and accelerated cell apoptosis. In addition, lncRNA PART1 induced downstream genes expression in TLR pathways including TLR3, TNFSF10 and CXCL13 to further influence prostate cancer cells, indicating its carcinogenesis on prostate cancer. LncRNA PART1 promoted cell proliferation ability and apoptosis via the inhibition of TLR pathways in prostate cancer. LncRNA PART1 could hence be considered as a new target in the treatment of prostate cancer.

Overexpression of Rab5a promotes hepatocellular carcinoma cell proliferation and invasion via FAK signaling pathway.

Rab5a was reported to be overexpressed in human malignancy and associated with the malignant phenotype. To data, its expression pattern and biological function in hepatocellular carcinoma (HCC) have not been studied. We analyzed Rab5a protein expression in 98 cases of HCC tissues and four HCC cell lines. We found that Rab5a expression was upregulated in HCC tissues and cell lines. Rab5a overexpression correlated with TNM stage and nodal metastasis (p < 0.05). To confirm the biological function of Rab5a in HCC cell lines, Rab5a siRNA was employed in SK-Hep-1 cell line and plasmid transfection was performed in Huh7 cell line. CCK-8 assay showed that Rab5a depletion blocked cell growth rate while Rab5a overexpression facilitated proliferation. Transwell and migration assay showed that Rab5a positively regulated cell invasion and migration. To explore the molecular mechanism underlying the biological effects of Rab5a, we checked several signaling pathways and found that Rab5a overexpression upregulated cyclin D1, cyclin E expression, FAK (Tyr397), and AKT (Ser473) phosphorylation. Blockage of FAK using inhibitor PF573228 abolished the role of Rab5a on cyclin D1. In conclusion, Rab5a is overexpressed in human HCC and contributes to cancer cell proliferation and invasion through regulation of FAK and AKT signaling.

Overexpression of Rab25 promotes hepatocellular carcinoma cell proliferation and invasion.

Rab25 was reported to be associated with several human cancers and malignant biological behavior of cancer cells. The goal of the present study was to determine its expression pattern and biological function in human hepatocellular carcinoma (HCC). We examined Rab25 protein in 92 cases of HCC tissues and 3 HCC cell lines. The results showed that Rab25 was upregulated in HCC tissues and cells compared with normal liver tissues and cell line. Rab25 overexpression correlated with advanced tumor stage and nodal metastasis. Rab25 small interfering RNA (siRNA) was employed in Bel7402 and SK-Hep-1 cell lines. Cell Counting Kit-8 (CCK-8) assay and colony formation assay showed that Rab25 depletion blocked cell growth rate and inhibited colony formation ability. Transwell assay showed that Rab25 depletion negatively regulated the invading ability of HCC cells. To explore the possible mechanisms, we checked several signaling pathways and found that Rab25 depletion downregulated AKT phosphorylation. In addition, luciferase reporter assay showed that Rab25 depletion inhibited the Wnt signaling pathway and its target genes such as cyclin D1, c-myc, and MMP7. In conclusion, Rab25 is overexpressed in human HCC and contributes to cancer cell proliferation and invasion possibly through regulation of the Wnt signaling pathway.

Upregulation of IRS-1 expression in Goto-Kakizaki rats following Roux-en-Y gastric bypass surgery: resolution of type 2 diabetes?

Type 2 diabetes mellitus (T2DM) is an endocrine disorder that is rapidly growing in prevalence within China and throughout the world. Roux-en-Y gastric bypass (RYGB) surgery, widely used in the treatment of obesity, has been recognized as an effective and long-term treatment for T2DM in recent years. However, the underlying mechanisms responsible for glycemic control remain unclear. This study was designed to investigate the roles of insulin receptor substrates (IRSs) in glucose tolerance and insulin resistance following RYGB surgery. Goto-Kakizaki (GK) rats, a model of T2DM, were randomly allocated into three groups: RYGB surgery, sham surgery, and control (10 animals/group). Wistar rats were also used as non-diabetic control. Daily food intake, body weight, glucose and insulin were measured pre- and post-operatively. Insulin receptor substrate 1 (IRS-1) and insulin receptor substrate 2 (IRS-2) content, the main subtypes of IRSs, were measured in skeletal muscle, adipose tissue and liver using western immunoblot analyses on postoperative day 28. Following surgery, RYGB-treated rats showed markedly improved oral glucose tolerance, as judged by lower peak and area-under-the-curve glucose values (p < 0.01 vs. GK or GK sham). Improved insulin resistance was also observed in RYGB-treated rats. Western immunoblot analyses showed that IRS-1 and its phosphorylation levels were significantly increased in skeletal muscle and adipose tissues in RYGB group (p < 0.01 vs. GK or GK sham), whereas IRS-2 levels were downregulated in liver. These findings suggest that improvements in glucose tolerance and insulin resistance following RYGB surgery are associated with upregulation of IRS-1.

Sleeve gastrectomy prevents lipoprotein receptor-1 expression in aortas of obese rats.

AIM: To investigate the effects of sleeve gastrectomy on adipose tissue infiltration and lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) expression in rat aortas. METHODS: Twenty-four rats were randomized into three groups: normal chow (control), high fat diet (HD) and high fat diet with sleeve gastrectomy (SG). After surgery, the HD and SG groups were fed a high fat diet. Animals were sacrificed and plasma high density lipoprotein (HDL) and low density lipoprotein (LDL) levels were determined. LOX-1 protein and LOX-1 mRNA expression was also measured. Aortas were stained with Nile red to visualize adipose tissue. RESULT: Body weights were higher in the HD group compared to the other groups. HDL levels in control, HD, and SG groups were 32.9 ± 6.2 mg/dL, 43.4 ± 4.0 mg/dL and 37.5 ± 4.3 mg/dL, respectively. LDL levels in control, HD, and SG groups were 31.8 ± 4.5 mg/dL, 53.3 ± 5.1 mg/dL and 40.5 ± 3.7 mg/dL, respectively. LOX-1 protein and LOX-1 mRNA expression was greater in the HD group versus the other groups. Staining for adipose tissue in aortas was greater in the HD group in comparison to the other groups. Thus, a high fat diet elevates LOX-1 protein and mRNA expression in aorta. CONCLUSION: Sleeve gastrectomy decreases plasma LDL levels, and downregulates LOX-1 protein and mRNA expression.

Roux-en-Y gastric bypass-induced improvement of glucose tolerance and insulin resistance in type 2 diabetic rats are mediated by glucagon-like peptide-1.

BACKGROUND: The aim of this study was to investigate the effects of Roux-en-Y gastric bypass (RYGB) on glucose tolerance and insulin resistance in type 2 diabetic rats and the possible mechanisms involved in this process. METHODS: Thirty Goto-Kakizaki (GK) rats were randomly divided into three groups: RYGB operation, sham operation, and food restriction groups. Ten Wistar rats were used as non-diabetic control. The body weight and food consumption of rats were recorded 1 week before or every week after surgery. The fasting blood sugar and oral glucose tolerance test were performed using blood glucose meter. The levels of plasma insulin or glucagon-like peptide-1 (GLP-1) were evaluated by enzyme-linked immunosorbent assay. The insulin resistance was quantified using homeostasis model assessment method. The expression of GLP-1 receptor, Bcl-2, Bax, and caspase-3 was determined by Western blotting. RESULTS: Our results revealed that RYGB efficiently improved both glucose tolerance and insulin resistance in GK diabetic rats by upregulating GLP-1/GLP-1R expression. In addition, GLP-1R agonist exendin-4 dose-dependently increased insulin secretion in RIN-m5F cells and regulated the proliferation and apoptosis of these cells. CONCLUSIONS: RYGB provides a valuable therapeutic option for patients with type 2 diabetes. GLP-1 may contribute to the regulation of pancreatic ß-cell function through its receptor following RYGB.

Adiponectin downregulates hyperglycemia and reduces pancreatic islet apoptosis after roux-en-y gastric bypass surgery.

BACKGROUND: The resolution of type 2 diabetes mellitus is an additional outcome of Roux-en-Y gastric bypass (RYGB) surgery. The general objective was to explore whether RYGB could reduce beta cells apoptosis and what roles adiponectin played in downregulating hyperglycemia after RYGB. METHODS: Twenty Goto-Kakizaki (GK) rats were allocated in RYGB group (ten) and GK group (ten), and ten Wistar (WS) rats were allocated in WS group. RYGB was performed in RYGB group and sham operation in the GK and WS groups. Fasting plasma glucose, body weight, food intake per 100 g body weight, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), C peptide, and adiponectin were measured pre- and postoperatively. Terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick end-labeling and transmission electron microscopy were performed to detect apoptosis of pancreatic beta cells. Data were analyzed by analysis of variance, Student t test, and post hoc comparisons (Tukey's test). RESULTS: Animals in WS group had significant higher postprandial insulin, C peptide, and adiponectin concentrations compared to RYGB and GK groups preoperatively. Body weight and food intake in RYGB group significantly decreased compared to WS and GK groups postoperatively. Postprandial insulin, C peptide, and adiponectin concentrations significantly increased, while fasting plasma glucose and HOMA-IR values decreased in RYGB group compared to GK group postoperatively. More apoptotic beta cells were detected in GK group than RYGB and WS groups postoperatively. CONCLUSIONS: RYGB could increase postprandial insulin and reduce pancreatic islet apoptosis. Adiponectin played a key role in regulating plasma glucose and reducing pancreatic islet apoptosis after RYGB.