Objective This article aims to assess the effects of ginger (Zingiber officinale Roscoe) on type 2 diabetes mellitus (T2DM) and/or components of the metabolic syndrome (MetS). Methods Electronic literature was searched in PubMed, Embase, the Cochrane Library, Chinese Biomedical Database, China National Knowledge Infrastructure, and Wanfang Database from inception of the database to May 19, 2017, and supplemented by browsing reference lists of potentially eligible articles. Randomized controlled trials on research subjects were included. Data were extracted as a mean difference (MD) and 95% confidence interval (CI). Subgroup analysis of fasting blood glucose (FBG) was performed. Results 10 studies met the inclusion criteria with a total of 490 individuals. Ginger showed a significant beneficial effect in glucose control and insulin sensitivity. The pooled weighted MD of glycosylated hemoglobin (HbA1c) was −1.00, (95% CI: −1.56, −0.44; P < 0.001). Subgroup analysis revealed that ginger obviously reduced FBG in T2DM patients (−21.24; 95% CI: −33.21, −9.26; P < 0.001). Meanwhile, the significant effects of improvement of lipid profile were observed. Most analyses were not statistically heterogeneous. Conclusion Based on the negligible side effects and obvious ameliorative effects on glucose control, insulin sensitivity, and lipid profile, ginger may be a promising adjuvant therapy for T2DM and MetS.

Level II-prognostic.

BackgroundLaparoscopic adrenalectomy has become the gold-standard for the surgical treatment of most adrenal lesions. This study evaluated the operative outcome of laparoendoscopic single-site (LESS) retroperitoneoscopic adrenalectomy (LESS-ARA) in comparison with the current standard operation procedure.MethodsBetween June and December 2009, 19 patients underwent LESS-ARA, and their outcomes were compared with a contemporary 1:2 matched-pair cohort of 38 patients who underwent standard ARA by the same surgeon. In LESS-ARA, a multichannel port was inserted through a 2.5- to 3.0-cm transverse skin incision below the tip of the 12th rib. The LESS-ARA procedure was performed using a 5-mm 30º laparoscopic camera and two standard laparoscopic instruments. The following parameters were compared between the two groups: demographics, details of the surgery, perioperative complications, postoperative visual analog pain scale score, analgesic requirement, and short-term measures of convalescence.ResultsThe finding showed that LESS-ARA and standard ARA were comparable in terms of the estimated blood loss (30 vs 17.5 ml; p = 0.64), postoperative hospital stay (6 vs 6 days; p = 0.67), and postoperative complications (2 vs 3 patients; p = 1.00) for patients with similar baseline demographics and median tumor size (2.1 vs 3.0; p = 0.18) cm. The intraoperative hemodynamic values were similar in the two groups. The LESS-ARA group had a longer median operative time (55 vs 41.5 min; p = 0.0004), whereas the in-hospital use of analgesics was significantly less (5 vs 12 morphine equivalents; p = 0.03).ConclusionsThe LESS retroperitoneoscopic adrenalectomy approach is feasible and offers a superior cosmetic outcome and better pain control, with perioperative outcomes and short-term measures of convalescence similar to those of the standard approach, albeit with a longer operative time.

γ-Aminobutyric acid (GABA) is produced by various cells through the catalytic activity of glutamic acid decarboxylase (GAD). Activation of type-A GABA receptor (GABAR) inhibits stem cell proliferation but protects differentiated cells from injures. The present study investigated hepatic GABA signaling system and the role of this system in liver physiology and pathophysiology. RT-PCR and immunoblot assays identified GAD and GABAR subunits in rat livers and in HepG2 and Clone 9 hepatocytes. Patch-clamp recording detected GABA-induced currents in Clone 9 hepatocytes and depolarization in WITT cholangiocytes. The function of hepatic GABA signaling system in rats was examined using models of d-galactosamine (GalN)-induced acute hepatocytic injury in vivo and in vitro. The expression of GAD increased whereas GABAR subunits decreased in the liver of GalN-treated rats. Remarkably, treating rats with GABA or the GABAR agonist muscimol, but not the GABAR agonist baclofen, protected hepatocytes against GalN toxicity and improved liver function. In addition, muscimol treatment decreased the formation of pseudobile ductules and the enlargement of hepatocytic canaliculi in GalN-treated rats. Our results revealed that a complex GABA signaling system exists in the rat liver. Activation of this intrahepatic GABAergic system protected the liver against toxic injury. Auto- and paracrine GABAergic signaling systems exist in the rat hepatocytes and cholangiocytes. Activation of GABA signaling protects liver function from d-galactosamine injury by reducing toxic impairment of hepatocytes and by decreasing cholangiocyte proliferation.