“
“Synechococcus- and Prochlorococcus-specific narB genes that encode for an assimilatory nitrate reductase are found in coastal to open-ocean waters. However, it remains uncertain if these picocyanobacteria assimilate nitrate in situ.

This unknown can potentially be addressed by examining narB mRNA from the environment, but this requires a better understanding of the influence of environmental factors on narB gene transcription. In laboratory experiments with Synechococcus sp. CC9311 cultures exposed to diel light fluctuations and grown on nitrate or ammonium, there was periodic change in narB transcript abundance. This periodicity was broken in cultures subjected to a doubling of irradiance (40–80 μmol photons · m−2 · s−1) learn more during the mid-light period. Therefore, the irradiance level, not circadian rhythm, was the dominant factor controlling

MK0683 mw narB transcription. In nitrate-grown cultures, diel change in narB transcript abundance and nitrate assimilation rate did not correlate; suggesting narB mRNA levels better indicate nitrate assimilation activity than assimilation rate. Growth history also affected narB transcription, as changes in narB mRNA levels in nitrogen-deprived CC9311 cultures following nitrate amendment were distinct from cultures grown solely on nitrate. Environmental sampling for narB transcripts should consider time, irradiance, and the growth status of cells to ecologically interpret narB transcript abundances. “
“The siphonous green algal family Caulerpaceae includes the monotypic genus Caulerpella and the species-rich genus Caulerpa. A molecular phylogeny was inferred from chloroplast tufA and rbcL DNA sequences analyzed together with a five marker dataset of non-caulerpacean siphonous green algae. Six Caulerpaceae lineages were revealed, but relationships between them remained largely unresolved. A Caulerpella clade representing multiple cryptic species was nested within CYTH4 the genus Caulerpa. Therefore, that genus is subsumed and Caulerpa ambigua Okamura is

reinstated. Caulerpa subgenus status is proposed for the six lineages substantiated by morphological characters, viz., three monotypic subgenera Cliftonii, Hedleyi, and Caulerpella, subgenus Araucarioideae exhibiting stolons covered with scale-like appendages, subgenus Charoideae characterized by a verticillate branching mode, and subgenus Caulerpa for a clade regarded as the Caulerpa core clade. The latter subgenus is subdivided in two sections, i.e., Sedoideae for species with pyrenoids and a species-rich section Caulerpa. A single section with the same name is proposed for each of the other five subgenera. In addition, species status is proposed for Caulerpa filicoides var. andamanensis (W.R. Taylor). All Caulerpa species without sequence data were examined (or data were taken from species descriptions) and classified in the new classification scheme. A temporal framework of Caulerpa diversification is provided by calibrating the phylogeny in geological time.

The correlation of MGd1-Ag and clinical parameters of gastric cancer patients was analyzed, and the role of MGd1-Ag in predicting the prognosis of gastric cancer was also studied. Trametinib price Results: Positive staining of MGd1-Ag was found in normal lung tissue, hematopoietic cells, esophageal squamous epithelial surface, colonic epithelium, mucus glands of the salivary glands, basal cell of

skin and few glandular lumens of breast tissue. Gastric, colorectal, pancreatic, and lung cancers showed abundant distribution of MGd1-Ag. It was positive in several cases of intestinal metaplasia and atypical hyperplasia tissues. The expression density of MGd1-Ag was significantly higher in gastric cancer of such situations including poor differentiation, advanced TNM staging and lymph node metastasis. The total positive rate of MGd1-Ag was 81.8% in gastric cancers. Kaplan-Meier

SB203580 clinical trial analysis and Log-rank test showed that increased MGd1-Ag expression in gastric cancer patients associated with poor outcomes. Conclusion: MGd1-Ag was specifically expressed in gastrointestinal cancers. It was increased in intestinal metaplasia and atypical hyperplasia, and, in gastric cancer, was correlated with grades of differentiation, TNM staging and lymph node metastasis. Increased MGd1-Ag expression in gastric cancer patients associated with poor outcomes. Key Word(s): 1. Gastric cancer; 2. Early diagnosis; 3. MGd1-Ag; 4. Prognosis; Presenting Author: RAVINDRA SATARASINGHE Additional Authors: RATHNAYAKE JAYEWARDENE, SATHYAJITH AMBAWATTE, NAYOMISHERMILA JAYASINGHE, RAVI WIJESINGHE, PUBUDU DE SILVA, NARTHANI RASENDRAN Corresponding Author: RAVINDRA SATARASINGHE Affiliations: Sri Jayewardenepura General Hospital Objective: To study the demographics and other related matters in a cohort of adult Sri Lankans having oesophageal varices. Methods: Case notes of upper gastrointestinal endoscopies of consecutive patients admitted to the principle author’s unit at Sri Jayewardenepura General Hospital, Kotte, Sri Lanka from 15th of February 2002 to 15th February 2013 were retrospectively analyzed

to obtain the required information. Results: Out of 2728 endoscopy findings analyzed, 599 had oesophageal Oxymatrine varices (22%). Sex distribution Male: Female was 5: 1. Alcoholic: non alcoholic was 7: 3. Mean age of the population was 56.1 ± 12.5 SD years. Only one female patient found to have varices secondary to alcoholic liver disease. Banding had been done in 37.2%. Prophylactic banding alone was done in 4.2%. Indications for upper gastrointestinal endoscopy had been haematamesis, variceal surveillance, malena and isolated portal hypertension in 29.5%, 29.5%, 22.5% and 10.7% respectively with overlaps. Sclerotherapy alone was offered in 13.9%. Follow up was effected only in 11.7% with rebanding in 21.5% within 3 to 6 months. Conclusion: Sex discrimination was less marked in non-alcoholics. Upper gastrointestinal bleeding was the commonest presentation.

Once again, determining whether this is a general characteristic this website of southern vs. northern false killer whales is difficult given the lack of systematically recorded data. Unfortunately there is no information on age or maturation

status for the animals from the 1936 St. Helena Bay stranding and 14 were unsexed. Nevertheless, adopting 3.25 m as the mean length of the female at maturation, and (as an upper limit) assuming all unsexed individuals between this length and 4.5 m (the largest female measured) were mature females, there would be a minimum of 17 and a maximum of 26 mature females in the school. Smithers (1938) recorded the presence of a 0.58 m fetus and one individual less than 2.8 m long (a calf of 1.57 m) which was presumably the only whale NVP-AUY922 solubility dmso of suckling age. These observations indicate that the incidence of fetuses and individuals of suckling size was between 2/26 (7.7%) and 2/17 (11.8%), depending on whether the upper or lower estimates of the number of mature females is adopted. These values are closer to the same statistic for the 1981 school (1/34 or 2.9%) than for those from Japan (23/67 or 34.3%). Nevertheless, it is not clear how thoroughly the 1936 whales were examined for fetuses, so their

incidence could be underestimated. In another mass stranding of false killer whales in South Africa (200–300 animals at Sea Spray, near Mamre, in November 1935), G. W. Rayner, a member of the Discovery Investigations,

and scientists from the South African Museum examined 18 females for the presence of a fetus but found none. Rayner commented that the females must all have calved shortly before stranding, although no newborn calves were found amongst the stranded animals (Birkby 1935). Different methods of estimating annual pregnancy rates, different possible criteria for establishing pregnancy and inherent biases (for example, representativeness of the sample), precluded a substantive comparison of the pregnancy rates reported in this study with those of other delphinids. However, the apparent pregnancy rates of false killer N-acetylglucosamine-1-phosphate transferase whales in this study, as well as elsewhere (10%–17%, Purves and Pilleri 1978), are lower than those estimated for 28 populations of eight other species of delphinids, which apart from a single value of 13.7% (for a killer whale population) fall within the range of 26.5%–80.4% (Perrin and Reilly 1984). Nevertheless, the apparently low reproductive rates of the three false killer whale schools from South Africa are remarkable. Although survival rates have not been calculated, it is obvious that they would have to be extremely high for the population to be biologically viable. Assuming an equal sex ratio at birth, the annual pregnancy rate of 2.2% calculated for the school stranded in 1981 and reported here equates to only 1.

Once again, determining whether this is a general characteristic LGK974 of southern vs. northern false killer whales is difficult given the lack of systematically recorded data. Unfortunately there is no information on age or maturation

status for the animals from the 1936 St. Helena Bay stranding and 14 were unsexed. Nevertheless, adopting 3.25 m as the mean length of the female at maturation, and (as an upper limit) assuming all unsexed individuals between this length and 4.5 m (the largest female measured) were mature females, there would be a minimum of 17 and a maximum of 26 mature females in the school. Smithers (1938) recorded the presence of a 0.58 m fetus and one individual less than 2.8 m long (a calf of 1.57 m) which was presumably the only whale selleck chemicals of suckling age. These observations indicate that the incidence of fetuses and individuals of suckling size was between 2/26 (7.7%) and 2/17 (11.8%), depending on whether the upper or lower estimates of the number of mature females is adopted. These values are closer to the same statistic for the 1981 school (1/34 or 2.9%) than for those from Japan (23/67 or 34.3%). Nevertheless, it is not clear how thoroughly the 1936 whales were examined for fetuses, so their

incidence could be underestimated. In another mass stranding of false killer whales in South Africa (200–300 animals at Sea Spray, near Mamre, in November 1935), G. W. Rayner, a member of the Discovery Investigations,

and scientists from the South African Museum examined 18 females for the presence of a fetus but found none. Rayner commented that the females must all have calved shortly before stranding, although no newborn calves were found amongst the stranded animals (Birkby 1935). Different methods of estimating annual pregnancy rates, different possible criteria for establishing pregnancy and inherent biases (for example, representativeness of the sample), precluded a substantive comparison of the pregnancy rates reported in this study with those of other delphinids. However, the apparent pregnancy rates of false killer Methane monooxygenase whales in this study, as well as elsewhere (10%–17%, Purves and Pilleri 1978), are lower than those estimated for 28 populations of eight other species of delphinids, which apart from a single value of 13.7% (for a killer whale population) fall within the range of 26.5%–80.4% (Perrin and Reilly 1984). Nevertheless, the apparently low reproductive rates of the three false killer whale schools from South Africa are remarkable. Although survival rates have not been calculated, it is obvious that they would have to be extremely high for the population to be biologically viable. Assuming an equal sex ratio at birth, the annual pregnancy rate of 2.2% calculated for the school stranded in 1981 and reported here equates to only 1.

Once again, determining whether this is a general characteristic Lorlatinib research buy of southern vs. northern false killer whales is difficult given the lack of systematically recorded data. Unfortunately there is no information on age or maturation

status for the animals from the 1936 St. Helena Bay stranding and 14 were unsexed. Nevertheless, adopting 3.25 m as the mean length of the female at maturation, and (as an upper limit) assuming all unsexed individuals between this length and 4.5 m (the largest female measured) were mature females, there would be a minimum of 17 and a maximum of 26 mature females in the school. Smithers (1938) recorded the presence of a 0.58 m fetus and one individual less than 2.8 m long (a calf of 1.57 m) which was presumably the only whale this website of suckling age. These observations indicate that the incidence of fetuses and individuals of suckling size was between 2/26 (7.7%) and 2/17 (11.8%), depending on whether the upper or lower estimates of the number of mature females is adopted. These values are closer to the same statistic for the 1981 school (1/34 or 2.9%) than for those from Japan (23/67 or 34.3%). Nevertheless, it is not clear how thoroughly the 1936 whales were examined for fetuses, so their

incidence could be underestimated. In another mass stranding of false killer whales in South Africa (200–300 animals at Sea Spray, near Mamre, in November 1935), G. W. Rayner, a member of the Discovery Investigations,

and scientists from the South African Museum examined 18 females for the presence of a fetus but found none. Rayner commented that the females must all have calved shortly before stranding, although no newborn calves were found amongst the stranded animals (Birkby 1935). Different methods of estimating annual pregnancy rates, different possible criteria for establishing pregnancy and inherent biases (for example, representativeness of the sample), precluded a substantive comparison of the pregnancy rates reported in this study with those of other delphinids. However, the apparent pregnancy rates of false killer Regorafenib in vitro whales in this study, as well as elsewhere (10%–17%, Purves and Pilleri 1978), are lower than those estimated for 28 populations of eight other species of delphinids, which apart from a single value of 13.7% (for a killer whale population) fall within the range of 26.5%–80.4% (Perrin and Reilly 1984). Nevertheless, the apparently low reproductive rates of the three false killer whale schools from South Africa are remarkable. Although survival rates have not been calculated, it is obvious that they would have to be extremely high for the population to be biologically viable. Assuming an equal sex ratio at birth, the annual pregnancy rate of 2.2% calculated for the school stranded in 1981 and reported here equates to only 1.

PPI-induced bacterial overgrowth, the presence of which is controversial,[58-60] may be also affected by duodenal H2O2 production. NSAID-induced enteropathy is associated with bacterial translocation.[61] PPI pretreatment aggravates NSAID-induced enteropathy by inducing dysbiosis,[62] suggesting that disruption of sterility in the foregut lumen by inhibition of PG synthesis combined with gastric acid suppression may also induce bacterial overload in the hindgut lumen, with resultant dysbiosis. Enteric pathogens such as salmonella, campylobacter, or listeria possess catalase activity. Helicobacter pylori,

a unique pathogen limited to the gastric mucosa, also possesses catalase and superoxide dismutase activity, as BAY 57-1293 mw one explanation for its long-term survival in situ. Pathogenic bacteria can resist the deleterious effects of H2O2, gastric acid and bile acid, whereas some commensal bacteria and eukaryotes such as fungi and yeast are H2O2 sensitive.[63, 64] Therefore, relative sterility of the duodenal lumen may be achieved by duodenal epithelial H2O2 production in addition to gastric acid and bile acid toxicity. The duodenal mucosa also senses luminal nutrients via nutrient sensors in order to rapidly control gastric emptying, bile

and pancreatic secretion, and intrinsic mucosal defenses through augmented ion secretion.[1, 65] Since luminal bacteria may disrupt nutrient sensors by taking up nutrients or by their metabolites interfering with nutrient detection, Duox2-mediated H2O2 release may repel enough bacteria from the epithelial surface, enhancing nutrient chemosensing and nutrient-evoked mucosal www.selleckchem.com/products/ch5424802.html responses.[66] Luminal nutrients may also be important instigators of anti-bacterial foregut mucosal responses. Duodenal bacterial overload

potentiates mucosal secretory responses,[67] further suggesting that the luminal bacterial environment affects the duodenal physiology. In conclusion, acid-induced PG synthesis may be mediated by luminal ATP-P2Y signals, Duox2-mediated H2O2 production, and cPLA2 activation, followed by COX activation. Released PGE2 stimulates basolateral EP4 receptors, augmenting protective HCO3− secretion via CFTR activation. This pathway forms one of the most important regulatory schemes coordinating duodenal mucosal defense mechanisms in response to luminal acid. Furthermore, the PG pathway, including anti-bacterial H2O2 production is also an important component of foregut mucosal defenses. Therefore, the duodenal PG pathway not only protects the foregut from mucosal injury, but also contributes to host defenses to luminal dysbiosis. We thank Drs Masaaki Higashiyama, Izumi Kaji, and David Strugatsky for their research contributions, and Ms. Bea Palileo for her assistance with manuscript preparation. Supported by a research grant from Department of Veterans Affairs Merit Review Award (JD Kaunitz) and NIH-NIDDK R01 DK54221 (JD Kaunitz).

[374, 377-381] 85. The role of LT in NCPH should be considered in those patients with cardiopulmonary complications of portal hypertension. (2-B) LT has been successfully

performed in a small number of children and adults with advanced liver disease in the setting of sickle cell anemia, but morbidity from vascular thrombosis including graft thrombosis, stroke or pulmonary embolus, and infections is common.[382-384] Vaso-occlusive crises continue after LT.[384] Careful patient selection as well as management of the sickle cell disease, including exchange transfusion, is required in order to successfully perform LT in patients with this systemic MEK inhibitor disorder. Hepatopulmonary syndrome (HPS) is a condition in which intrapulmonary vascular dilatations (IPVD) develop in the setting of portal systemic shunting.[385] The presence of HPS is associated with increased morbidity and mortality,[386] but is generally reversible after transplantation and is not a contraindication for transplantation.[387] ACP-196 molecular weight HPS is present in 4 to 29% chronic liver disease patients of all ages.[43, 388, 389] Among patients with biliary

atresia, HPS may occur more commonly in children with splenic malformation syndrome.[125, 381] It is important to recognize that HPS can occur in patients without evidence of liver dysfunction (e.g., congenital hepatic fibrosis, portal vein thrombosis, cavernous Oxymatrine transformation of the portal vein). The diagnosis of HPS in children is confirmed by the presence of hypoxia and one of the following

demonstrating the presence of IPVD: 1) contrast-enhanced transthoracic echocardiography; 2) technetium-labeled macro-aggregated albumin lung perfusion scan demonstrating a shunt fraction of >6%; or 3) cardiac catheterization demonstrating IPVD.[44] Severe shunting of >20%, as determined by macro-aggregated albumin scan, is associated with increased posttransplantation morbidity and mortality in adults.[44, 386] The median survival in the absence of LT in adults with severe HPS (paO2 <50 mmHg) is less than 12 months, but is unknown in children.[390-392] Patients with HPS may benefit from supplemental oxygen, particularly during periods of increased physical activity.[12] LT is appropriate for the treatment of HPS in children with cirrhotic liver disease and may be appropriate in some noncirrhosis patients with HPS. Noncirrhotic liver disease or congenital/acquired portosystemic venous communications (e.g., Abernathy syndrome) resulting in HPS may present opportunities for alternative nontransplant approaches to management.[387, 393-396] These approaches include ligation of the shunt or endovascular treatment using an occlusion device placed by an interventional radiologist. 86.

[374, 377-381] 85. The role of LT in NCPH should be considered in those patients with cardiopulmonary complications of portal hypertension. (2-B) LT has been successfully

performed in a small number of children and adults with advanced liver disease in the setting of sickle cell anemia, but morbidity from vascular thrombosis including graft thrombosis, stroke or pulmonary embolus, and infections is common.[382-384] Vaso-occlusive crises continue after LT.[384] Careful patient selection as well as management of the sickle cell disease, including exchange transfusion, is required in order to successfully perform LT in patients with this systemic selleck screening library disorder. Hepatopulmonary syndrome (HPS) is a condition in which intrapulmonary vascular dilatations (IPVD) develop in the setting of portal systemic shunting.[385] The presence of HPS is associated with increased morbidity and mortality,[386] but is generally reversible after transplantation and is not a contraindication for transplantation.[387] learn more HPS is present in 4 to 29% chronic liver disease patients of all ages.[43, 388, 389] Among patients with biliary

atresia, HPS may occur more commonly in children with splenic malformation syndrome.[125, 381] It is important to recognize that HPS can occur in patients without evidence of liver dysfunction (e.g., congenital hepatic fibrosis, portal vein thrombosis, cavernous aminophylline transformation of the portal vein). The diagnosis of HPS in children is confirmed by the presence of hypoxia and one of the following

demonstrating the presence of IPVD: 1) contrast-enhanced transthoracic echocardiography; 2) technetium-labeled macro-aggregated albumin lung perfusion scan demonstrating a shunt fraction of >6%; or 3) cardiac catheterization demonstrating IPVD.[44] Severe shunting of >20%, as determined by macro-aggregated albumin scan, is associated with increased posttransplantation morbidity and mortality in adults.[44, 386] The median survival in the absence of LT in adults with severe HPS (paO2 <50 mmHg) is less than 12 months, but is unknown in children.[390-392] Patients with HPS may benefit from supplemental oxygen, particularly during periods of increased physical activity.[12] LT is appropriate for the treatment of HPS in children with cirrhotic liver disease and may be appropriate in some noncirrhosis patients with HPS. Noncirrhotic liver disease or congenital/acquired portosystemic venous communications (e.g., Abernathy syndrome) resulting in HPS may present opportunities for alternative nontransplant approaches to management.[387, 393-396] These approaches include ligation of the shunt or endovascular treatment using an occlusion device placed by an interventional radiologist. 86.

, Hercules, CA). Caspase-3 activity was measured by enzyme-linked immunosorbent assay (ELISA) using the ApoAlert Caspase-3 colorimetric assay kit from Clontech Laboratories, Inc. (Mountain View, CA).6 In addition, apoptotic cell death was assessed in the cultured cholangiocarcinoma cell lines by DNA laddering, as described,6 and by detection with fluorescence microscopy of nuclear fragmentation in 4′,6-diamidino-2-phenylindole (DAPI) nuclear stained preparations. Animal experimentation was performed in accordance with criteria outlined in the Guide for the Care and Use of Laboratory Animals,9 using protocols

approved by the Institutional Animal selleck chemical Care and Use Committee at Virginia Commonwealth University. Briefly, 4 × 106 BDEneu cells (viability ≥ 90%) were inoculated into the bile ducts of syngeneic young adult male Fischer 344 rats as described.4 Rats were randomized twice before being designated as either “treated” or “control”. The treated group was administered lapatinib at 75 mg/kg of body weight given by gavage twice a day for a period of 24-26 days. The control group received the

vehicle only, composed SCH772984 solubility dmso of 0.5% (wt/wt) hydroxypropyl methylcellulose and 0.1% (wt/wt) Tween-80 in distilled water, according to the same treatment schedule as the lapatinib-treated group. Treatment was initiated at either 2 days (early treatment) or 8 days (late treatment) after bile duct inoculation of the BDEneu cells. All animals were weighed once a day in the morning before the start of a daily treatment. At the conclusion of the treatment period, the rats were sacrificed, and gross hepatic tumor incidence and liver tumor wet weights were determined for

both the vehicle-treated control and lapatinib-treated groups. Serum samples were obtained from blood collected by cardiac puncture at the time of sacrifice and flash frozen for total bilirubin assessment using the QuantiChrome Bilirubin Assay Kit (DIBR-80) purchased from BioAssay Systems (Hayward, CA). Flash frozen cryopreserved tumor samples were also obtained at sacrifice and used to assess, by immunohistochemistry and western blotting, the effect of Oxalosuccinic acid lapatinib treatment on ErbB2 tyrosine 1248 (Tyr1248) phosphorylation, as described.4 Mean values ± standard deviation (SD) were calculated and the Student two-tailed t test was used to determine P values, with a P value of ≤ 0.05 considered significant. The synergistic effects of AG879 in combination with AG1517 on in vitro cell growth inhibition was determined by the combination index (CI) method.10 A CI value < 1 indicated synergism. Relative expression levels of ErbB1 and ErbB2 proteins in the two rat and two human cholangiocarcinoma cell lines employed in this study were determined by western blotting. As shown in Fig. 1, the four different cholangiocarcinoma cell lines analyzed expressed variable levels of p170 ErbB1 and p185 ErbB2.

Equal volumes of plasma from mice of the same genotype were pooled and 200 μL of

the pooled plasma was applied to a Superose 6L HR 10/30 column (GE Healthcare, Baie d’Urfe, Quebec, Canada) with 154 mM NaCl, 1 mM ethylene diamine tetraacetic acid (pH 8). Fractions were assayed using modified protocols of the Cholesterol E kit and Serum Triglyceride Determination INK 128 mw kit. Sodium dodecyl sulfate–polyacrylamide gel electrophoresis was performed on 1 μL of plasma or 15 μL of fast protein liquid chromatography eluate using a 4%-15% gradient gel. Polyvinylidene fluoride membranes were probed with an apoB antibody that detects both apoB48 and apoB100 (K23300R; Meridian Life Science, Saco, ME). Quantitative polymerase chain reaction for apoB, hepatic lipase, and LPL is described in detail in the Supporting Information. Liver lysates were prepared and assessed for LPL and non-LPL activity as described in the Supporting Information. Livers were fixed in

4% paraformaldehyde overnight and stored in 70% ethanol. Sections (5 μm) were stained with hematoxylin and eosin and visualized under oil immersion. Four-hour fasted mice were given 5 μL/g olive oil via oral gavage. Plasma samples were taken over 5 hours and assayed for triglycerides. We first determined whether triglyceride output from the liver was altered in the fasting state. To evaluate

selleck chemicals find more VLDL triglyceride secretion from the liver, we injected fasted mice with poloxamer-407. Poloxamer-407 was a potent inhibitor of triglyceride uptake (Fig. 1A), but the accumulation in plasma triglycerides occurred at similar rates in Leprflox/flox AlbCre+ mice and their Leprflox/flox AlbCre− littermate controls. Because insulin suppresses VLDL triglyceride secretion17 and the livers of Leprflox/flox AlbCre+ mice are more sensitive to the effects of insulin,13 we examined whether a bolus of insulin could differentially affect VLDL triglyceride secretion in these mice. In response to insulin, there was a decreased rate of plasma triglyceride accumulation in both Leprflox/flox AlbCre+ mice and littermate controls (Figs. 1B,C). Surprisingly, in Leprflox/flox AlbCre+ mice, there were elevated levels of plasma triglycerides after insulin injection compared with controls (Figs. 1B,C), suggesting that insulin mediated suppression of triglyceride secretion is muted in mice lacking hepatic leptin signaling. We next investigated the effects of hepatic leptin signaling on fasting plasma triglycerides under more strenuous metabolic conditions. Leprflox/flox AlbCre mice were crossed onto an obese, hyperinsulinemic ob/ob background to generate ob/ob mice lacking functional hepatic leptin receptors (Leprflox/flox AlbCre ob/ob mice).