Short-Term Changes on Body Composition After Sleeve Gastrectomy and One Anastomosis Gastric Bypass.

Introduction: Changes in body composition after different bariatric surgeries have been studied extensively, but most of them have emphasized on Roux-en-Y gastric bypass. Only a few studies have assessed the effects of sleeve gastrectomy (SG). Also, the effect of one anastomosis gastric bypass (OAGB) on body composition is not fully apprehended. Furthermore, there is no agreement on how much fat-free mass (FFM) loss is tolerable in weight loss interventions. Therefore, we decided to assess the reduction in fat mass (FM) and FFM at 1, 3, 6, and 12 months after two types of bariatric surgery in a single center. Methods: In the current retrospective cross-sectional study, the patients' hospital records were analyzed. We included patients who had SG or OAGB and a complete 1-year follow-up record. We recorded demographic data as well as weight, body mass index (BMI), FM, and FFM before and at 1, 3, 6, and 12 months after surgery in a predesigned checklist. Results: We analyzed 311 patients (43 males and 268 females) in the SG (N = 192, 61.7%) and OAGB (N = 119, 38.3%) groups. Both the SG and OAGB groups demonstrated a statistically significant reduction in weight, BMI, FM, and FFM indices at 12 months after the intervention (P < .001). Moreover, no statistically significant difference was observed between the SG and OAGB groups regarding the mean of all body composition indices at 3, 6, and 12 months after the intervention. Conclusion: We found that SG and OAGB effectively decreased weight and body composition indices, comprising FM and FFM, with no significant difference between each other.

Rosiglitazone and a ß3-Adrenoceptor Agonist Are Both Required for Functional Browning of White Adipocytes in Culture.

The recruitment of brite (or beige) adipocytes has been advocated as a means to combat obesity, due to their ability to phenotypically resemble brown adipocytes (BA). Lineage studies indicate that brite adipocytes are formed by differentiation of precursor cells or by direct conversion of existing white adipocytes, depending on the adipose depot examined. We have systematically compared the gene expression profile and a functional output (oxygen consumption) in mouse adipocytes cultured from two contrasting depots, namely interscapular brown adipose tissue, and inguinal white adipose tissue (iWAT), following treatment with a known browning agent, the peroxisome proliferator-activated receptor (PPARγ) activator rosiglitazone. Prototypical BA readily express uncoupling protein (UCP)1, and upstream regulators including the ß3-adrenoceptor and transcription factors involved in energy homeostasis. Adipocytes from inguinal WAT display maximal UCP1 expression and mitochondrial uncoupling only when treated with a combination of the PPARγ activator rosiglitazone and a ß3-adrenoceptor agonist. In conclusion, brite adipocytes are fully activated only when a browning agent (rosiglitazone) and a thermogenic agent (ß3-adrenoceptor agonist) are added in combination. The presence of rosiglitazone throughout the 7-day culture period partially masks the effects of ß3-adrenoceptor signaling in inguinal white adipocyte cultures, whereas including rosiglitazone only for the first 3 days promotes robust ß3-adrenoceptor expression and provides an improved window for detection of ß3-adrenoceptor responses.

The PPARγ agonist rosiglitazone promotes the induction of brite adipocytes, increasing ß-adrenoceptor-mediated mitochondrial function and glucose uptake.

Recruitment and activation of brite (or beige) adipocytes has been advocated as a potential avenue for manipulating whole-body energy expenditure. Despite numerous studies illustrating the differences in gene and protein markers between brown, brite and white adipocytes, there is very little information on the adrenergic regulation and function of these brite adipocytes. We have compared the functional (cyclic AMP accumulation, oxygen consumption rates, mitochondrial function, glucose uptake, extracellular acidification rates, calcium influx) profiles of mouse adipocytes cultured from three contrasting depots, namely interscapular brown adipose tissue, and inguinal or epididymal white adipose tissues, following chronic treatment with the peroxisome proliferator-activated receptor γ (PPARγ) agonist rosiglitazone. Prototypical brown adipocytes readily express ß3-adrenoceptors, and ß3-adrenoceptor stimulation increases cyclic AMP accumulation, oxygen consumption rates, mitochondrial function, glucose uptake, and extracellular acidification rates. Treatment of brown adipocytes with rosiglitazone increases uncoupling protein 1 (UCP1) levels, and increases ß3-adrenoceptor mitochondrial function but does not affect glucose uptake responses. In contrast, inguinal white adipocytes only express UCP1 and ß3-adrenoceptors following rosiglitazone treatment, which results in an increase in all ß3-adrenoceptor-mediated functions. The effect of rosiglitazone in epididymal white adipocytes, was much lower compared to inguinal white adipocytes. Rosiglitazone also increased α1-adrenoceptor mediated increases in calcium influx and glucose uptake (but not mitochondrial function) in inguinal and epididymal white adipocytes. In conclusion, the PPARγ agonist rosiglitazone promotes the induction and function of brite adipocytes cultured from inguinal and epididymal white adipose depots.

Sublethal exposures of diazinon alters glucose homostasis in Wistar rats: Biochemical and molecular evidences of oxidative stress in adipose tissues.

Disorder of glucose homeostasis is one of the most important complications following exposure to organophosphorous (OPs) pesticides. Regarding the importance of adipose tissue in regulating blood glucose and the role of oxidative stress in toxicity of OPs and in the continue of our previous works, in the present study we focused on tumor necrosis factor alpha (TNFα), glucose transporter type 4 (GLUT4), and nuclear factor kappa-light-chain-enhancer of activated B cells (Nf-κB) in a sublethal model of toxicity by diazinon as a common OPs. Following time-course study of various doses of diazinon in impairing blood glucose, dose of 70mg/kg/day was found the optimum. Animals were treated for 4 weeks and after gavage of glucose (2g/kg), the glucose change was evaluated at time-points of 0, 30, 60, 120 and 180min to identify oral glucose tolerance test (GTT). In addition, serum insulin was measured in fasting condition. In adipose tissue, oxidative stress markers including reactive oxygen species (ROS), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and TNFα were evaluated. The mRNA expression of GLUT4, Nf-κB and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were also determined by real time reverse transcription polymerase chain reaction (RT-PCR). Diazinon at dose of 70mg/kg/day impaired GTT and diminished insulin level while augmented ROS, NADPH oxidase, and TNFα. The GLUT4 mRNA expression was amplified by diazinon while unlikely, the expression of Nf-κB gene did not change. On the basis of biochemical and molecular findings, it is concluded that diazinon impairs glucose homeostasis through oxidative stress and related proinflammatory markers in a way to result in a reduced function of insulin inside adipose tissue. Although, diazinon interfered with pancreatic influence on the adipose tissue most probably via stimulation of muscarinic receptors, current data are not sufficient to introduce adipose tissue as a target organ to OPs toxicity. Considering the potential of OPs to accumulate in adipose tissue, it seems a good candidate organ for future studies. Although, hyperglycemia was not induced by diazinon but increased AUC0-180min leads us to the point that diazinon induces kind of instability in glucose homostasis and diabetes.

Polymyositis as presenting manifestation of gallbladder carcinoma: A case report.

INTRODUCTION: Inflammatory myositis as a paraneoplastic presentation of gallbladder cancer is an extremely rare event. In this paper we reported the first case of gallbladder carcinoma presented as polymyositis. PRESENTATION OF CASE: A 68-year-old housewife presented with proximal muscles weakness, pain, significant decrease in force of proximal muscles, and globally decreased deep tendon reflexes. Laboratory studies revealed an anemia, increased acute phase reactants and increased serum creatine phosphokinase (CPK) levels. Electromyography (EMG) and nerve conduction velocity test (NCV) demonstrated mild myopathic changes. Muscle biopsy was suggestive for polymyositis. Corticosteroid therapy initiated and a meticulous search for probable underlying malignancy performed concurrently. Malignancy workup finally revealed a gallbladder tumor. Patient candidated for extended cholecystectomy. Pathologic evaluation of gallbladder tumor demonstrated a moderately differentiated carcinoma. Progressive improvement in clinical conditions and complete normalization of laboratory parameters occurred post-operatively. After 8 months of follow-up patient is still alive and in good state of health. There is no evidence of metastatic or local recurrence of tumor. Musculoskeletal complaints subsided completely. DISCUSSION: Gallbladder carcinoma is a rare and usually aggressive malignancy. Its primary presentation by paraneoplastic syndromes especially in the form of paraneoplastic neurological syndromes is an extremely rare event. Some believes that increased association between inflammatory myopathy and malignancy is limited to the dermatomyositis; however, presentation of our patient as polymyositis is contrary to this. This is the first reported case of gallbladder cancer who presented with polymyositis. CONCLUSION: Gallbladder cancer though rare, should be considered in patients with inflammatory myositis.

Gross hematuria as the presentation of an inguinoscrotal hernia: a case report.

INTRODUCTION: Several complications have been reported with inguinal hernias. Although hematuria and flank pain, either as the presentation or as a complication of inguinal hernia, are infrequent, this condition may lead to the development of obstructive uropathy, which can have diverse manifestations. CASE PRESENTATION: A 71-year-old Iranian man with Persian ethnicity presented with new onset episodes of gross hematuria and left-sided flank pain. A physical examination revealed a large and non-tender inguinal hernia on his left side. An initial workup included an abdominal ultrasound, an intravenous pyelogram and cystoscopy, which showed left hydronephrosis and a bulging on the left-side of his bladder wall. On further evaluation, computed tomography confirmed that his sigmoid colon was the source of the pressure effect on his bladder, resulting in hydroureteronephrosis and hematuria. No tumoral lesion was evident. Herniorrhaphy led to the resolution of his signs and symptoms. CONCLUSION: Our case illustrates a rare presentation of inguinal hernia responsible for gross hematuria and unilateral hydronephrosis. Urologic signs and symptoms can be caused by the content of inguinal hernias. They can also present as complications of inguinal hernias.

Biochemical and cellular evidence of the benefit of a combination of cerium oxide nanoparticles and selenium to diabetic rats.

AIM: To study the combinative effects of nanocerium and selenium in a murine model of diabetes. METHODS: Cerium oxide (CeO(2)) nanoparticles (60 mg/kg per day) and sodium selenite (5 µmol/kg per day) alone or in combination, or the metal form of CeO(2) (60 mg/kg) were administered for 2 wk by intraperitoneal injection to streptozotocin-induced diabetic rats. At the end of treatment blood was collected, liver tissue dissected and then oxidative stress markers, extent of energy depletion and lipid profile were evaluated. RESULTS: Antioxidant enzymes and high density lipoprotein decreased whereas oxidative stress, adenosine diphosphate/adenosine triphospahte levels, cholesterol, triglyceride and low density lipoprotein increased on induction of diabetes. All were improved by a combination of nanocerium and sodium selenite. There was a relative amelioration by CeO(2) nanoparticles or sodium selenite alone, but the metal form of CeO(2) showed no significant improvement. CONCLUSION: The combination of nanocerium and sodium selenite is more effective than either alone in improving diabetes-induced oxidative stress.