Abdominal Banding Research Articles

Notes on the Occurrence of Abnormal Thoracic and Abdominal Banding in Culex territans Larvae (Diptera: Culicidae).

Pale-banded variants of Culex territans Walker larvae were found in southern New Jersey in 2016 and in subsequent years. The larvae lacked pigmentation on the prothoracic and mesothoracic segments as well as on abdominal segment (IV). The amount of pigmentation varied between populations. Specimens were found in six locations within a 5-yr period; of which, two locations recurred within the same season and in subsequent seasons. This is the first report in the State of New Jersey despite extensive larval surveillance over many years among the study area.

Candesartan Cilexetil Attenuates Arrhythmogenicity Following Pressure Overload in Rats via the Modulation of Cardiac Electrical and Structural Remodeling and Calcium Handling Dysfunction.

BackgroundCardiac hypertrophy is associated with abnormal electrophysiology and increased arrhythmia risk. This study assessed whether candesartan cilexetil, an angiotensin II type 1 receptor blocker, could suppress arrhythmogenecity by attenuating cardiac electrical remodeling and calcium mishandling in rats with pressure‐overload hypertrophy.Methods and ResultsMale Sprague‐Dawley rats were randomly subjected to abdominal aorta banding or sham procedure and received either candesartan cilexetil (3.0 mg/kg per day) or vehicle by gavage for 5 weeks. Pressure overload was characterized by compensated left ventricular (LV) hypertrophy and fibrosis, increased LV pressure and its decay time, and prolonged corrected QT interval, all of which were attenuated by candesartan cilexetil treatment. Candesartan cilexetil–treated banded rat hearts displayed shorter QT intervals and lower vulnerability to atrial and ventricular tachyarrhythmias than vehicle‐treated banded hearts. Candesartan cilexetil prevented banding‐induced prolonged action potential duration and reduced the occurrence of triggered activity in LV papillary muscles. In addition, the prolonged time to 50% cell relengthening and calcium transient decay time were normalized in LV myocytes from candesartan cilexetil–treated banded rats, along with a normalization of decreased SERCA2a (sarco[endo]plasmic reticulum calcium‐ATPase) expression in LV tissues. Furthermore, candesartan cilexetil normalized depressed transient outward potassium current densities and protein and mRNA levels of both voltage‐gated potassium 4.2 and 4.3 channel subunits (Kv4.2 and Kv4.3) in banded rats.ConclusionsCandesartan cilexetil protects the heart from pressure overload‐induced adverse electrical remodeling by preserving potassium channel densities. In addition, calcium handling and its molecular regulation also improved after treatment. These beneficial effects may contribute to a lower susceptibility to arrhythmias in hearts from candesartan cilexetil–treated pressure‐overloaded rats.

Effect of low wall shear stress on the morphology of endothelial cells and its evaluation indicators

ObjectiveThis study is designed to explore the morphological changes of endothelial cells (ECs) under different levels of shear stress and find the effective evaluation indicators with in vivo and in vitro experiments. MethodsHuman umbilical vein endothelial cells (HUVECs) and Sprague–Dawley rats were used to study the effect of different shear stress which applied by means of parallel plate-flow chamber and abdominal aorta banding model on the morphology of endothelial cells. Then, fluorescence images were acquired by means of a confocal laser-scanning microscope. Finally, Cell morphological indicators were extracted by SRAD-MCW computer image processing algorithm for quantitative analysis. Results1) The morphological changes of HUVECs were observed after exposure to shear stress for 6 h, the HUVECs were elongated and spindle-shaped. And the degree of cell deformability was different while the exposure time was different, then it became stable after 18 h. The HUVECs exposure to high shear stress (HSS) exhibited an ordered cell arrangement, while the HUVECs exposure to low shear stress (LSS) showed a disordered cell arrangement. 2) Traditional cell morphological indicators such as area, perimeter, long axis diameter, short axis diameter and orientation angle were not significantly different between the normal shear stress (NSS) group and the LSS group (P > 0.05), but the intercellular space characteristics such as the junction length per unit area and the triple points per unit area were significantly different (P < 0.05). ConclusionThese results demonstrate that the size and duration of shear stress can affect the morphology and arrangement of endothelial cells. The commonly used evaluation indicators for studying the effect of shear stress on the morphology of endothelial cells, including area, perimeter, long axis diameter, short axis diameter and orientation angle, etc., had no significant statistical significance, while the intercellular space characteristics including the junction length per unit area and the triple points per unit area can be used as effective indicator to study the effect of shear stress on the morphology of endothelial cells.

Abdominal esophageal banding for esophageal atresia with tracheoesophageal fistula in neonates with severe associated anomalies.

The aim of this study was to evaluate the materials used for abdominal esophageal banding, and to evaluate the complications associated with abdominal esophageal banding. The medical records of seven patients with esophageal atresia (EA) and tracheoesophageal fistula (TEF) who underwent abdominal esophageal banding between December 2009 and January 2020 were retrospectively reviewed. The patients were banded with vinyl tape (n = 1), silicone tape (n = 2), polyacetal resin clips (n = 1), or an expanded polytetrafluoroethylene (ePTFE) sheet (n = 3). Banding with vinyl tape resulted in banding failure at postoperative day (POD) 89. One patient with silicone tape developed banding failure at POD 177. In the other patient, it was discovered during radical surgery that the silicone tape had slipped through the abdominal esophagus. Polyacetal resin clip banding resulted in esophageal wall perforation at POD 27. One patient banded with an ePTFE sheet underwent upper gastric transection at POD 650, while another underwent TEF resection at POD 156; in the third patient, the banding condition was maintained for more than 100days. Abdominal esophageal banding is useful as a palliative treatment for EA/TEF with severe associated anomalies. Surgeons should plan the next surgery depending on the patient's condition.

Effects of Lycium barbarum L. Polysaccharides on Inflammation and Oxidative Stress Markers in a Pressure Overload-Induced Heart Failure Rat Model.

Despite recent advances in disease management and prevention, heart failure (HF) prevalence is still high. Hypertension, inflammation and oxidative stress are being investigated as important causative processes in HF. L. barbarum L. polysaccharides (LBPs) are widely used for their anti-inflammatory and antioxidant properties. Thus, the aim of the present study was to evaluate the effects of LBPs on inflammation and oxidative stress markers in a pressure overload-induced HF rat model, surgically induced by abdominal aorta banding in Wistar rats (AAB) (n = 28). Also, control rats (n = 10) were subjected to a sham operation. After echocardiographic confirmation of HF (week 24), AAB rats were divided into three groups: rats treated with LBPs for 12 weeks: 100 mg/kg body weight /day (AAB_100, n = 9), 200 mg/kg body weight /day (AAB_200, n = 7) and no-treatment group (control AAB, n = 12). After 12 weeks of treatment with LBPs, the decline of cardiac function was prevented compared to the control AAB rats. Treatment with 200 mg/kg body weight /day LBPs significantly reduced the inflammation as seen by cytokine levels (IL-6 and TNF-α) and the plasma lipid peroxidation, as seen by malondialdehyde levels. These results suggest that LBPs present anti-inflammatory and antioxidant effects with utility in a HF animal model and encourage further investigation of the cardioprotective effects of these polysaccharides.

Drosophila hegdii (Diptera: Drosophilidae), a new species from Lumami, Nagaland (a sub-Himalayan hilly state, India): Its molecular phylogeny

Survey for Drosophila was carried out in Lumami (which is a hamlet in Zunheboto district of Nagaland and is head quarters of the Nagaland University) and Drosophila hegdii was one among the 16 species collected. Based on the morphological markers, internal characters a new species, Drosophila hegdii, was identified. Drosophila hegdii resembles Drosophila vulcana and Drosophila jambulina in certain morphological markers, but differed with them in multiple morphological markers. It also differs from other known species of montium sub group in characters such as the number of teeth in sex comb, and abdominal banding pattern. In order to confirm new species status with the aid of molecular markers and decipher molecular phylogeny we took advantage of “DNA Barcoding” by analysing sequences of mitochondrial cytochrome c oxidase subunit I (COI) (its 648 base pair fragment is the standard marker for “species identification” in the Barcode of Life Project). Neighbour joining trees were constructed using MEGA5 (Neighbor-Joining Tree (NJ) method with bootstrap test-1000 replicates) using the Kimura 2-parameter model, with gaps treated by pairwise deletion. Molecular phylogeny confirms the observations made with the help of morphological markers that Drosophila hegdii is a new species and closer to Drosophila vulcana and Drosophila jambulina.

Resveratrol Suppresses Cardiac Renin Angiotensin System in the Late Phase of Left Ventricular Hypertrophy

Background and objectives: Resveratrol(3,5,4′-trihydroxy-trans-stilbene) is a natural polyphenole phytoalexin which exerts potential cardioprotective effects, but the cellular and molecular mechanisms responsible for these effects are still unknown. Cardiac renin angiotensin system (RAS) over-activation plays an important role in pathogenesis of left ventricular hypertrophy (LVH) progression. The aim of the study was to investigate the effects of resveratrol on the main components of RAS during early and late phase of myocardial hypertrophy. Methods: To consider the early and late phase of LVH, the rats were studied two and sixteen weeks after abdominal aorta banding without treatment (H2w and H16w groups, respectively) or with resveratrol (R) treatment. Intact animals served as control (Ctl). Arterial blood pressure was recorded by carotid cannulation. Angiotensin II (Ang II) level was measured using ELISA kit. Gene expression was evaluated by Real time RT-PCR technique. Cardiomyocyte size and fibrosis were assessed using haematoxylin/eosin and Masson trichrome staining, respectively Results: Results of this study showed that in H2w group AT1a mRNA level was increased significantly (pConclusion: Progression of LVH is accompanied by dynamic changes in RAS components expression in myocardial tissue. Resveratrol protects the heart against pressure overload-induced hypertrophy in part via RAS suppression.

Carvacrol Ameliorates Pathological Cardiac Hypertrophy in Both In-vivo and In-vitro Models.

Hypertension-induced left ventricular hypertrophy is the most important risk factor for heart failure. This study aimed at investigating the effects of monoterpenoid phenol, carvacrol, on myocardial hypertrophy using both in-vivo and in-vitro models. Male Wistar rats were divided into the control (Ctl), un-treated hypertrophy (H), and carvacrol-treated hypertrophy groups (25, 50 and 75 mg/kg/day, Car+H). In the hypertrophy groups animals underwent abdominal aorta banding. Blood pressure (BP) was recorded via carotid artery cannulation. TUNEL assay and Masson’s trichrome staining were used to assess apoptosis and fibrosis, respectively. The 2-2-diphenyl 1-picril-hydrasil )DPPH( radical scavenging activity and malondialdehyde (MDA) level were estimated by biochemical tests. In in-vitro study H9c2 cardiomyoblasts were treated with angiotensin II (Ang II) to promote hypertrophy. Cell size was measured using crystal violet staining. Gene expression was evaluated by real-time RT-PCR technique. In the carvacrol-treated rats BP, heart rate, and heart weight to the body weight ratio were significantly decreased. In-vitro study showed that H9c2 cell size was significantly reduced compared to Ang II-treated cells. Both in-vivo and in-vitro studies demonstrated that carvacrol decreased atrial natriuretic peptide )ANP( mRNA level significantly (vs. H groups). The number of apoptotic cells increased in H group, while it was decreased in the Car50+H and Car75+H. In Car+H groups, in comparison with H group, the serum concentration of MDA was decreased and DPPH was increased significantly. Our findings demonstrated that carvacrol decreases hypertrophy markers in in-vivo and in-vitro models of hypertrophy.

Morphological and molecular evidence for a new species of Lutzia (Diptera: Culicidae: Culicini) from Thailand

We found a species of LutziaTheobald (1903) (Diptera: Culicidae) in Chiang Mai Province and other provinces in northern Thailand which bears morphological and DNA sequence differences from the three species of Lutzia, subgenus Metalutzia Tanaka, previously recorded from Thailand, namely Lt. fuscana (Wiedemann), Lt. halifaxii (Theobald) and Lt. vorax Edwards. The adults of the Chiang Mai form (CM form) have abdominal banding patterns similar to those of Lt. vorax from Japan (which includes the type locality of this species), but differ in having the mediocubital crossvein usually positioned before rather than beyond the radiomedial crossvein. The thoracic and abdominal integument of Lt. vorax larvae is covered with relatively short pointed spicules whereas it is covered by denser, longer and more acutely pointed spicules in the CM form. Some differences are also found in the development of thoracic seta 1-M, and abdominal setae 8-II and 8-III. The pupa of the CM form clearly differs from the pupa of Lt. vorax in having setae 1 and 5 of abdominal segments V and VI branched rather than single. The characters of the wing, larva and pupa of the CM form are similar to those of Lt. fuscana and Lt. halifaxii. However, whereas the phallosome of males of the CM form is similar to males of Lt. vorax and Lt. halifaxii, it is distinct from males of Lt. fuscana. Phylogenetic analysis of mitochondrial cytochrome c oxidase subunits I and II sequences revealed that the CM form falls outside a clade comprised of specimens of Lt. vorax from Japan, Korea, Thailand and Bhutan (Kimura 2-parameter, K2P, genetic distances 3.9–5.6, and 5.1–6.6, respectively). However, the two gene sequences of the CM form are not clearly distinct from clades comprised of sequences from specimens of Lt. fuscana and Lt. halifaxii (K2P 0.2–2.4%). However, based on the combination of morphological and molecular data, the current study provides evidence that the CM form is a previously unrecognized species of the genus Lutzia.

Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway.

Cardiac hypertrophy is characterized by a shift in metabolic substrate utilization, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline. The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats. Cardiomyocyte size and cardiac fibrosis were significantly increased in hypertrophic hearts. In vitro cardiomyocyte hypertrophy was induced by exposing neonatal rat cardiomyocytes to angiotensin II (Ang II) (10-6 M, 24 h). Choline attenuated the mito-nuclear protein imbalance and activated the mitochondrial-unfolded protein response (UPRmt) in the heart, thereby preserving the ultrastructure and function of mitochondria in the context of cardiac hypertrophy. Moreover, choline inhibited myocardial metabolic dysfunction by promoting the expression of proteins involved in ketone body and fatty acid metabolism in response to pressure overload, accompanied by the activation of sirtuin 3/AMP-activated protein kinase (SIRT3-AMPK) signalling. In vitro analyses demonstrated that SIRT3 siRNA diminished choline-mediated activation of ketone body metabolism and UPRmt, as well as inhibition of hypertrophic signals. Intriguingly, serum from choline-treated abdominal aorta banding models (where β-hydroxybutyrate was increased) attenuated Ang II-induced myocyte hypertrophy, which indicates that β-hydroxybutyrate is important for the cardioprotective effects of choline. Choline attenuated cardiac dysfunction by modulating the expression of proteins involved in ketone body and fatty acid metabolism, and induction of UPRmt; this was likely mediated by activation of the SIRT3-AMPK pathway. Taken together, these results identify SIRT3-AMPK as a key cardiac transcriptional regulator that helps orchestrate an adaptive metabolic response to cardiac stress. Choline treatment may represent a new therapeutic strategy for optimizing myocardial metabolism in the context of hypertrophy and heart failure.

A Case of Type C Esophageal Atresia Wherein Retained Abdominal Esophageal Banding Tape Was Endoscopically Removed

A Case of Type C Esophageal Atresia Wherein Retained Abdominal Esophageal Banding Tape Was Endoscopically Removed

C 型食道閉鎖症における腹部食道 Banding 法の合併症と問題点について

C 型食道閉鎖症における腹部食道 Banding 法の合併症と問題点について

極小未熟児の C 型食道閉鎖症に対する食道 Banding 法の経験

極小未熟児の C 型食道閉鎖症に対する食道 Banding 法の経験

In Vivo and In Vitro Protective Effects of Pentamethylquercetin on Cardiac Hypertrophy

To investigate the in vivo and in vitro protective effects of pentamethylquercetin (PMQ), a member of polymethoxy flavonoids (PMFs), on cardiac hypertrophy. An in vivo cardiac hypertrophy model established by abdominal aorta banding technique in rats was treated with PMQ in increasing dosages (2.5, 5, and 10 mg x kg(-1) x d(-1)). An in vitro cardiomyocyte hypertrophy model was induced by treating neonatal cardiomyocytes with endothelin-1 (ET-1, 0.1 μM). An in vitro fibrosis model was developed in cardiac fibroblasts by aldosterone (Ald, 20 nM) and treated with PMQ (0.3, 1, 3 and 10 μM). Hemodynamic, morphological, histological, and biochemical changes were evaluated at corresponding time points. The abdominal aorta constriction (AAC) rats demonstrated a significantly elevated blood pressure and profound systolic and diastolic cardiac dysfunction. The resultant cardiac hypertrophy and heart failure were characterized by a significant increase in the heart and lung indices (3.51 ± 0.30 vs 2.35 ± 0.24, 5.58 ± 0.85 vs 3.94 ± 0.54; both P < 0.01), cardiomyocyte cross-sectional areas (153 ± 33% vs 100 ± 5%, P < 0.01) and myocardial fibrosis (9.09 ± 1.30% vs 1.49 ± 0.20%, P < 0.01) with concomitant elevation of B-type natriuretic peptide and cardiac collagen mRNA level. Daily oral administration of PMQ (2.5, 5, and 10 mg/kg for 7 weeks) prevented the foregoing histology, gene and protein changes secondary to AAC procedure. In addition, the up-regulated inflammation factors such as TNF-α and IL-6, and the down-regulated PPAR α and PPAR β were normalizd by PMQ treatment. PMQ has significant protective effects on cardiac hypertrophy through up-regulating the mRNA and protein levels of PPAR α and PPAR β involved in the process of inflammation response and cardiac fibrosis.

Noninvasive Detection of Coronary Artery Stenoses with Contrast-Enhanced Whole-Heart Coronary Magnetic Resonance Angiography at 3.0 T

Purpose: To prospectively evaluate the accuracy of contrast-enhanced whole-heart coronary magnetic resonance angiography (CMRA) at 3.0 T, with the use of sublingual nitroglycerin and abdominal banding, for assessing significant stenosis (≧50% lumen diameter reduction) in patients with suspected coronary disease, using conventional coronary artery angiography as the reference standard. Methods: We prospectively studied 71 consecutive patients with suspected coronary artery disease scheduled for conventional coronary angiography. Contrast-enhanced whole-heart CMRA was performed after sublingual nitroglycerin with an abdominal banding rolled tightly along the side of the ribs. The diagnostic performance of CMRA for the detection of significant lesions was compared with that of quantitative coronary angiography. Results: The acquisition of CMRA was completed in 67 of 71 patients, with an average imaging time of 9.6 ± 3.2 min. The average navigator efficiency was 48%. The sensitivity, specificity as well as positive and negative predictive values of whole-heart CMRA for the detection of significant lesions on a segment-by-segment analysis were 91.4, 85.8, 48.7 and 98.5%, respectively, and in a patient-based analysis 94.6, 86.7, 89.7 and 92.9%, respectively. Conclusions: Contrast-enhanced whole-heart CMRA with 3.0 T optimized by using sublingual nitroglycerin and abdominal banding methods permits reliable detection of significant obstructive coronary artery disease in patients with suspected coronary disease.

Pulse pressure variation and stroke volume variation during increased intra-abdominal pressure: an experimental study

IntroductionThe aim of this study was to evaluate dynamic indices of fluid responsiveness in a model of intra-abdominal hypertension.MethodsNine mechanically-ventilated pigs underwent increased intra-abdominal pressure (IAP) by abdominal banding up to 30 mmHg and then fluid loading (FL) at this IAP. The same protocol was carried out in the same animals made hypovolemic by blood withdrawal. In both volemic conditions, dynamic indices of preload dependence were measured at baseline IAP, at 30 mmHg of IAP, and after FL. Dynamic indices involved respiratory variations in stroke volume (SVV), pulse pressure (PPV), and systolic pressure (SPV, %SPV and Δdown). Stroke volume (SV) was measured using an ultrasound transit-time flow probe placed around the aortic root. Pigs were considered to be fluid responders if their SV increased by 15% or more with FL. Indices of fluid responsiveness were compared with a Mann-Whitney U test. Then, receiver operating characteristic (ROC) curves were generated for these parameters, allowing determination of the cut-off values by using Youden's method.ResultsFive animals before blood withdrawal and all animals after blood withdrawal were fluid responders. Before FL, SVV (78 ± 19 vs 42 ± 17%), PPV (64 ± 18 vs 37 ± 15%), SPV (24 ± 5 vs 18 ± 3 mmHg), %SPV (24 ± 4 vs 17 ± 3%) and Δdown (13 ± 5 vs 6 ± 4 mmHg) were higher in responders than in non-responders (P < 0.05). Areas under ROC curves were 0.93 (95% confidence interval: 0.80 to 1.06), 0.89 (0.70 to 1.07), 0.90 (0.74 to 1.05), 0.92 (0.78 to 1.06), and 0.86 (0.67 to 1.06), respectively. Threshold values discriminating responders and non-responders were 67% for SVV and 41% for PPV.ConclusionsIn intra-abdominal hypertension, respiratory variations in stroke volume and arterial pressure remain indicative of fluid responsiveness, even if threshold values identifying responders and non-responders might be higher than during normal intra-abdominal pressure. Further studies are required in humans to determine these thresholds in intra-abdominal hypertension.

A long-term survival case of tracheal agenesis: management for tracheoesophageal fistula and esophageal reconstruction

Tracheal agenesis is a very rare disorder which leads to severe respiratory disorders immediately after birth. Reports are very limited on long-term survival cases. We report here a long-term survival case with Floyd's type I tracheal agenesis. During the neonatal stage, the patient underwent abdominal esophageal banding to substitute esophagus for trachea and transection at the cervical esophagus with esophagostomy. Subsequently, airway management was difficult due to a fragile tracheoesophageal fistula, but the fistula was conservatively treated and stabilized with the patient's growth. This patient is a very rare case in whom oral feeding was achieved after esophageal reconstruction using a gastric tube. For this case, we describe mainly (1) the management method of the tracheoesophageal fistula and (2) esophageal reconstruction without thoracotomy.

Apocynin attenuates pressure overload-induced cardiac hypertrophy in rats by reducing levels of reactive oxygen species

It has been shown that angiotensin II (Ang II) is involved in cardiac remodeling mediated by NADPH oxidase-dependent reactive oxygen species (ROS). Accordingly, NADPH oxidase-dependent ROS may play a role in cardiac hypertrophy induced by pressure overload. In the present study, we sought to determine whether inhibition of NADPH oxidase prevents cardiac hypertrophy. After abdominal aorta banding to induce cardiac hypertrophy, rats were treated for 8 weeks with apocynin (Apo) or captopril (Cap). Measures of cardiac hypertrophy were evaluated. Treatment with Cap or Apo reduced the left ventricle/body weight ratio (LV/BW), LV transnuclear myocyte diameter, and atrial natriuretic factor (ANF) mRNA expression relative to those of untreated rats subjected to aorta banding. The activity of NADPH oxidase and the ROS levels were decreased in treated animals. Cap, but not Apo, decreased Ang II levels and inhibited expression of p22phox and p67phox in LVs. In conclusion, local expression of Ang II appears to contribute to pressure overload-induced cardiac hypertrophy by upregulating NADPH oxidase expression and promoting ROS synthesis. Inhibition of NADPH oxidase and elimination of ROS may prevent or repair damage due to cardiac hypertrophy.

Abstract 5398: Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) Supplementation, but not α-Linolenic Acid, Elevates Plasma Adiponectin Concentration and Prevents Pressure Overload Induced Ventricular Dysfunction and Remodeling

Coronary disease is reduced by intake of the ω-3 polyunsaturated fatty acids (ω-3PUFA) EPA and DHA. Recent evidence suggest EPA+DHA may also prevent development of heart failure. We previously showed that intake of fish oil rich in EPA+DHA up-regulates expression and plasma levels of adiponectin, a cardioprotective adipose-derived hormone. We examined the effects of dietary EPA+DHA on plasma adiponectin levels and development of left ventriclular (LV) dysfunction and remodeling in response to pressure overload induced by abdominal aorta banding. Rats were fed either a standard chow or diets supplemented with EPA+DHA from fish oil at 0.7%, 2.3% or 7% of energy intake. LV volumes were measured by echo. On the standard diet banding increased LV mass by 38%, LV end diastolic volume by 29%, and end diastolic volume by 101% compared to sham (p&lt;0.05). EPA+DHA supplementation increased plasma adiponectin concentration in a dose dependent manner (see Fig. ), and prevented the increases in LV end diastolic volume and end systolic volume (p&lt;0.05). Adiponectin levels were negatively correlated with LV end systolic and diastolic volumes (r=−0.78 and −0.71, respectively; p&lt;0.001). The protective effect of adiponectin has been linked to AMPK activation and/or inhibition of pro-growth Akt, however there were no differences in AMPK or Akt activation by western blot. A parallel series of rats were fed with α-linolenic acid, a ω-3PUFA from flaxseed, over a similar dose range, and showed no increase in adiponectin or prevention of LV pathology. In conclusion, supplementation with EPA+DHA prevented LV remodeling and dysfunction, which was strongly associated with an elevation in plasma adiponectin.

The common rs9939609 gene variant of the fat mass- and obesity-associated gene FTO is related to fat cell lipolysis

We investigated the rs9939609 single nucleotide polymorphism of the FTO gene in relation to fat cell function and adipose tissue gene expression in 306 healthy women with a wide range in body mass index (18-53 kg/m(2)). Subcutaneous adipose tissue biopsies were taken for fat cell metabolism studies and in a subgroup (n = 90) for gene expression analyses. In homozygous carriers of the T-allele, the in vitro basal (spontaneous) adipocyte glycerol release was increased by 22% (P = 0.007) and the in vivo plasma glycerol level was increased by approximately 30% (P = 0.037) compared with carriers of the A allele. In contrast, there were no genotype effects on catecholamine-stimulated lipolysis or basal or insulin-induced lipogenesis. We found no difference between genotypes for adipose tissue mRNA levels of FTO, hormone-sensitive lipase, adipose triglyceride lipase, perilipin, or CGI-58. Finally, the adipose tissue level of FTO mRNA was increased in obesity (P = 0.002), was similar in subcutaneous and omental adipose tissue, was higher in fat cells than in fat tissue (P = 0.0007), and was induced at an early stage in the differentiation process (P = 0.004). These data suggest a role of the FTO gene in fat cell lipolysis, which may be important in explaining why the gene is implicated in body weight regulation.