bluuebunny/crossref_metadata_2025_split huggingface dataset:
Elevated basal and post-feed glucagon-like peptide 1 (GLP-1) concentrations in the neonatal period
Authors: Padidela Raja , Patterson Michael , Sharief Nawfal , Ghatei Mohammed , Hussain Khalid 
Published: October 2008

BackgroundGlucagon-like peptide 1 (GLP-1) is an incretin hormone that stimulates glucose-induced insulin secretion, increases β-cell proliferation, neogenesis and β-cell mass. In adults, plasma concentrations of amidated GLP-1 are typically within the 5–10 pmol/l range in the fasting state and increases to ∼50 pmol/l after ingestion of a mixed meal.Research design and methodsWe measured plasma glucose, insulin and amidated forms of GLP-1 prefeed and then at 20 and 60 min post-feed following ingestion of a 60–70 ml of standard milk feed in preterm (n=10, 34–37 weeks) and term newborn infants (n=12, 37–42 weeks). Reverse-phase fast protein liquid chromatography was used to characterise the molecular nature of the circulating GLP-1.ResultsMean birth weight was 3.18 kg and mean age at sampling for GLP-1 was 7.7 days. The mean basal GLP-1 concentration was 79.1 pmol/l, which increased to 156.6 pmol/l (±70.9,P<0.001) and 121.5 pmol/l (±59.2) at 20 and 60 min respectively. Reverse-phase chromatography analysis suggested that the majority of GLP-1 immunoreactivity (>75%) represented GLP-1 (7–36) amide and (9–36) amide.ConclusionsBasal and post-feed amidated GLP-1 concentrations in neonates are grossly raised with the major fractions of circulating GLP-1 being (7–36) amide and (9–36) amide. Elevated GLP-1 concentrations in the newborn period may have a role in regulating maturation of enteroendocrine system and also of increasing pancreatic β-cell mass and regeneration. The high levels of GLP-1 may be due to immaturity of the dipeptidyl peptidase IV and or lower glomerular filtration rate in the neonatal period. Further studies are required to understand the role of GLP-1 in the neonatal period.
On the Interaction between Incisor Crown-Root Morphology and Third-Order Angulation
Authors: Knösel Michael , Jung Klaus , Attin Thomas , Engelke Wilfried , Kubein-Meesenburg Dietmar , Gripp-Rudolph Liliam , Attin Rengin 
Published: October 2008

Abstract
Objective: To evaluate the significance of crown-root angles (CRAs) by testing the null hypothesis that there are no significant differences in deviations of third-order angles to axial inclination values between Angle Class II division 2 incisors and a neutral occlusion control sample.
Materials and Methods: The study group comprised ntotal = 130 whites with either Angle Class II division 2 (n1 = 62; group A) or neutral (n2 = 68; control group B) occlusal relationships. Upper central incisor inclination (U1) was assessed with reference to the cephalometric lines NA and palatal plane (U1NA/deg, U1PP/deg). Craniofacial sagittal and vertical relations were classified using angles SNA, SNB, ANB, and NSL-PP. Third-order angles were derived from corresponding dental cast pairs using an incisor inclination gauge. Welch's two-sample t-tests (α-level: .05) were used to test the null hypothesis. Single linear regression was applied to determine third-order angle values as a function of axial inclination values (U1NA, U1PP) or sagittal craniofacial structures (ANB angle), separately for group A and B.
Results: The discrepancy between axial inclination (U1NA, U1PP) and third-order angles is significantly different (P &lt; .001) between groups A and B. Regression analysis revealed a simply moderate correlation between third-order measurements and axial inclinations or sagittal craniofacial structures.
Conclusion: The hypothesis is rejected. The results of this study warn against the use of identical third-order angles irrespective of diminished CRAs typical for Angle Class II division 2 subjects. Routine CRA assessment may be considered in orthodontic treatment planning of Angle Class II division 2 cases.
Skeletal Muscle–Specific Deletion of Lipoprotein Lipase Enhances Insulin Signaling in Skeletal Muscle but Causes Insulin Resistance in Liver and Other Tissues
Authors: Wang Hong , Knaub Leslie A. , Jensen Dalan R. , Young Jung Dae , Hong Eun-Gyoung , Ko Hwi-Jin , Coates Alison M. , Goldberg Ira J. , de la Houssaye Becky A. , Janssen Rachel C. , McCurdy Carrie E. , Rahman Shaikh M. , Soo Choi Cheol , Shulman Gerald I. , Kim Jason K. , Friedman Jacob E. , Eckel Robert H. 
Published: October 2008

OBJECTIVE
Skeletal muscle–specific LPL knockout mouse (SMLPL−/−) were created to study the systemic impact of reduced lipoprotein lipid delivery in skeletal muscle on insulin sensitivity, body weight, and composition.

RESEARCH DESIGN AND METHODS
Tissue-specific insulin sensitivity was assessed using a hyperinsulinemic-euglycemic clamp and 2-deoxyglucose uptake. Gene expression and insulin-signaling molecules were compared in skeletal muscle and liver of SMLPL−/− and control mice.

RESULTS
Nine-week-old SMLPL−/− mice showed no differences in body weight, fat mass, or whole-body insulin sensitivity, but older SMLPL−/− mice had greater weight gain and whole-body insulin resistance. High-fat diet feeding accelerated the development of obesity. In young SMLPL−/− mice, insulin-stimulated glucose uptake was increased 58% in the skeletal muscle, but was reduced in white adipose tissue (WAT) and heart. Insulin action was also diminished in liver: 40% suppression of hepatic glucose production in SMLPL−/− vs. 90% in control mice. Skeletal muscle triglyceride was 38% lower, and insulin-stimulated phosphorylated Akt (Ser473) was twofold greater in SMLPL−/− mice without changes in IRS-1 tyrosine phosphorylation and phosphatidylinositol 3-kinase activity. Hepatic triglyceride and liver X receptor, carbohydrate response element–binding protein, and PEPCK mRNAs were unaffected in SMLPL−/− mice, but peroxisome proliferator–activated receptor (PPAR)-γ coactivator-1α and interleukin-1β mRNAs were higher, and stearoyl–coenzyme A desaturase-1 and PPARγ mRNAs were reduced.

CONCLUSIONS
LPL deletion in skeletal muscle reduces lipid storage and increases insulin signaling in skeletal muscle without changes in body composition. Moreover, lack of LPL in skeletal muscle results in insulin resistance in other key metabolic tissues and ultimately leads to obesity and systemic insulin resistance.
Elevated Expression of Osteopontin May Be Related to Adipose Tissue Macrophage Accumulation and Liver Steatosis in Morbid Obesity
Authors: Bertola Adeline , Deveaux Vanessa , Bonnafous Stéphanie , Rousseau Déborah , Anty Rodolphe , Wakkach Abdelilah , Dahman Moncef , Tordjman Joan , Clément Karine , McQuaid Siobhán E. , Frayn Keith N. , Huet Pierre-Michel , Gugenheim Jean , Lotersztajn Sophie , Le Marchand-Brustel Yannick , Tran Albert , Gual Philippe 
Published: October 2008

OBJECTIVE—Osteopontin (OPN) plays an important role in the development of insulin resistance and liver complications in dietary murine models. We aimed to determine the expression pattern of OPN and its receptor CD44 in obese patients and mice according to insulin resistance and liver steatosis.
RESEARCH DESIGN AND METHODS—OPN and CD44 expressions were studied in 52 morbidly obese patients and in mice. Cellular studies were performed in HepG2 cells.
RESULTS—Hepatic OPN and CD44 expressions were strongly correlated with liver steatosis and insulin resistance in obese patients and mice. This increased OPN expression could be due to the accumulation of triglycerides, since fat loading in HepG2 promotes OPN expression. In contrast, OPN expression in adipose tissue (AT) was enhanced independently of insulin resistance and hepatic steatosis in obese patients. The elevated OPN expression in AT was paralleled with the AT macrophage infiltration, and both phenomena were reversed after weight loss. The circulating OPN level was slightly elevated in obese patients and was not related to liver steatosis. Further, AT did not appear to secrete OPN. In contrast, bariatric surgery–induced weight loss induced a strong increase in circulating OPN.
CONCLUSIONS—The modestly elevated circulating OPN levels in morbidly obese patients were not related to liver steatosis and did not appear to result from adipose tissue secretion. In subcutaneous AT, expression of OPN was directly related to macrophage accumulation independently from liver complications. In contrast, hepatic OPN and CD44 expressions were related to insulin resistance and steatosis, suggesting their local implication in the progression of liver injury.
Mid- and Late-Life Diabetes in Relation to the Risk of Dementia
Authors: Xu Weili , Qiu Chengxuan , Gatz Margaret , Pedersen Nancy L. , Johansson Boo , Fratiglioni Laura 
Published: October 2008

OBJECTIVE—We aimed to verify the association between diabetes and the risk of dementia, Alzheimer's disease, and vascular dementia in twins and to explore whether genetic and early-life environmental factors could contribute to this association.
RESEARCH DESIGN AND METHODS—This study included 13,693 twin individuals aged ≥65 years. Dementia was diagnosed according to DSM-IV (Diagnostic Manual of Mental Disorders, 4th ed.) criteria. Information on diabetes was collected from the inpatient registry and self- or informant-reported history of diabetes. Data were analyzed following two strategies: 1) unmatched case-control analysis for all participants using generalized estimating equation (GEE) models and 2) cotwin matched case-control analysis for dementia-discordant twin pairs using conditional logistic regression.
RESULTS—Of all participants, 467 were diagnosed with dementia, including 292 with Alzheimer's disease and 105 with vascular dementia, and an additional 170 were diagnosed with questionable dementia. Diabetes was present in 1,396 subjects. In GEE models, diabetes was associated with adjusted odds ratios (ORs) (95% CI) of 1.89 (1.51–2.38) for dementia, 1.69 (1.16–2.36) for Alzheimer's disease, and 2.17 (1.36–3.47) for vascular dementia. Compared with late-life diabetes (onset age ≥65 years), the risk effect of mid-life diabetes (onset age &lt;65 years) on dementia was stronger. Conditional logistic analysis of 210 dementia-discordant twin pairs led to ORs of 2.41 (1.05–5.51) and 0.68 (0.30–1.53) for dementia related to mid- and late-life diabetes, respectively.
CONCLUSIONS—Diabetes increases the risk of Alzheimer disease and vascular dementia. The risk is stronger when diabetes occurs at mid-life than in late life. Genetic and early-life environmental factors might contribute to the late-life diabetes–dementia association but could not account for the mid-life diabetes–dementia association.
Hepatic Stearoyl-CoA Desaturase (SCD)-1 Activity and Diacylglycerol but Not Ceramide Concentrations Are Increased in the Nonalcoholic Human Fatty Liver
Authors: Kotronen Anna , Seppänen-Laakso Tuulikki , Westerbacka Jukka , Kiviluoto Tuula , Arola Johanna , Ruskeepää Anna-Liisa , Orešič Matej , Yki-Järvinen Hannele 
Published: October 2008

OBJECTIVE—To determine whether 1) hepatic ceramide and diacylglycerol concentrations, 2) SCD1 activity, and 3) hepatic lipogenic index are increased in the human nonalcoholic fatty liver.
RESEARCH DESIGN AND METHODS—We studied 16 subjects with (n = 8) and without (n = 8) histologically determined nonalcoholic fatty liver (NAFL+ and NAFL−) matched for age, sex, and BMI. Hepatic concentrations of lipids and fatty acids were quantitated using ultra-performance liquid chromatography coupled to mass spectrometry and gas chromatography.
RESULTS—The absolute (nmol/mg) hepatic concentrations of diacylglycerols but not ceramides were increased in the NAFL+ group compared with the NAFL− group. The livers of the NAFL+ group contained proportionally less long-chain polyunsaturated fatty acids as compared with the NAFL− group. Liver fat percent was positively related to hepatic stearoyl-CoA desaturase 1 (SCD1) activity index (r = 0.70, P = 0.003) and the hepatic lipogenic index (r = 0.54, P = 0.030). Hepatic SCD1 activity index was positively related to the concentrations of diacylglycerols (r = 0.71, P = 0.002) but not ceramides (r = 0.07, NS).
CONCLUSIONS—We conclude that diacylglycerols but not ceramides are increased in NAFL. The human fatty liver is also characterized by depletion of long polyunsaturated fatty acids in the liver and increases in hepatic SCD1 and lipogenic activities.
Restoration of Hepatic Glucokinase Expression Corrects Hepatic Glucose Flux and Normalizes Plasma Glucose in Zucker Diabetic Fatty Rats
Authors: Torres Tracy P. , Catlin ReEtta L. , Chan Robert , Fujimoto Yuka , Sasaki Noriyasu , Printz Richard L. , Newgard Christopher B. , Shiota Masakazu 
Published: October 2008

OBJECTIVE—We examined in 20-week-old Zucker diabetic fatty (ZDF) rats whether restoration of hepatic glucokinase (GK) expression would alter hepatic glucose flux and improve hyperglycemia.
RESEARCH DESIGN AND METHODS—ZDF rats were treated at various doses with an adenovirus that directs the expression of rat liver GK (AdvCMV-GKL) dose dependently, and various metabolic parameters were compared with those of nondiabetic lean littermates (ZCL rats) before and during a hyperglycemic clamp. Viral infection per se did not affect hepatic GK activity, since expression of a catalytically inactive form of GK did not alter endogenous hepatic GK activity.
RESULTS—ZDF rats compared with ZCL rats have lower hepatic GK activity (11.6 ± 1.9 vs. 32.5 ± 3.2 mU/mg protein), marked hyperglycemia (23.9 ± 1.2 vs. 7.4 ± 0.3 mmol/l), higher endogenous glucose production (80 ± 3 vs. 38 ± 3 μmol · kg−1 · min−1), increased glucose-6-phosphatase flux (150 ± 11 vs. 58 ± 8 μmol · kg−1 · min−1), and during a hyperglycemic clamp, a failure to suppress endogenous glucose production (80 ± 7 vs. −7 ± 4 μmol · kg−1 · min−1) and promote glucose incorporation into glycogen (15 ± 5 vs. 43 ± 3 μmol/g liver). Treatment of ZDF rats with different doses of AdvCMV-GKL, which restored hepatic GK activity to one to two times that of ZCL rats, normalized plasma glucose levels and endogenous glucose production. During a hyperglycemic clamp, glucose production was suppressed and glucose incorporation into glycogen was normal.
CONCLUSIONS—Alteration of hepatic GK activity in ZDF rats has profound effects on plasma glucose and hepatic glucose flux.
Growth and market integration in Amazonia: A comparison of growth indicators between Shuar, Shiwiar, and nonindigenous school children
Authors: Blackwell Aaron D. , Pryor George , Pozo José , Tiwia Washington , Sugiyama Lawrence S. 
Published: October 2008

AbstractWe describe and compare the growth of three groups of juveniles, aged 0–18, who experience different degrees of market integration and acculturation in the Ecuadorian Amazon. These include 1,384 indigenous Shuar from the Upano Valley of Ecuador and surrounding areas, 570 nonindigenouscolono(or colonist) children from the same area, and 42 Shiwiar from the interior of Ecuador. We use differences between these populations in National Health and Nutrition Examination Survey (NHANES)z‐scores to assess the effects of changing subsistence patterns on Shuar growth and nutrition. Although, for all three groups, mean height‐for‐agez‐scores were negative, Shuarz‐scores were significantly lower than either colono or Shiwiarz‐scores. Mean weight‐for‐agez‐scores were also negative for Shuar and colono juveniles, while mean BMI‐for‐age and weight‐for‐heightz‐scores were greater than zero for all three groups. Using NHANES standards, 41% of male and 38% of female Shuar were classified as stunted, versus 16% of male and 20% of female colonos. Compared to Shuar, colonos were three times less likely to be stunted (OR = 0.33,P< 0.01) and Shiwiar were eight times less likely to be stunted (OR = 0.13,P= 0.01). These differences suggest that changes in diet have negatively affected Shuar growth and nutrition. Am. J. Hum. Biol, 2009. © 2008 Wiley‐Liss, Inc.
Evaluation of iron deficiency as a nutritional adaptation to infectious disease: An evolutionary medicine perspective
Authors: Wander Katherine , Shell‐Duncan Bettina , McDade Thomas W. 
Published: October 2008

AbstractAn evolutionary perspective suggests that iron deficiency may have opposing effects on infectious disease risk, decreasing susceptibility by restricting iron availability to pathogens, and increasing susceptibility by compromising cellular immunocompetence. In some environments, the trade‐off between these effects may result in optimal iron intake that is inadequate to fully meet body iron needs. Thus, it has been suggested that moderate iron deficiency may protect against acute infection, and may represent a nutritional adaptation to endemic infectious disease stress. To test this assertion, we examined the association between infection, reflected by C‐reactive protein, a biomarker of inflammation, and iron status, reflected by transferrin receptor (TfR) and zinc protoporphyrin to heme ratio (ZPP:H), among school‐age Kenyan children, and evaluated the hypothesis that moderate iron deficiency is associated with lower odds of infectious disease. TfR > 5.0 mg/l, with sensitivity and specificity for iron deficiency (ZPP:H > 80 μmol/mol) of 0.807 and 0.815, was selected as the TfR definition of iron deficiency. Controlling for age and triceps skinfold thickness (TSF), the odds ratio (OR) for acute viral or bacterial infection associated with iron deficiency (compared to normal/replete) was 0.50 (P= 0.11). Controlling for age and TSF, the OR for infection associated with an unequivocally iron replete state (compared to all others) was 2.9 (P= 0.01). We conclude that iron deficiency may protect against acute infection in children. Am. J. Hum. Biol, 2009. © 2008 Wiley‐Liss, Inc.
Contributions of Mouse Genetic Background and Age on Anterior Lens Capsule Thickness
Authors: Danysh Brian P. , Czymmek Kirk J. , Olurin Pecos T. , Sivak Jacob G. , Duncan Melinda K. 
Published: October 2008

AbstractAccurate lens capsule thickness measurements are necessary for studies investigating mechanical characteristics of the capsule. Confocal Z‐axis imaging was used to measure the anterior lens capsule thickness of living intact lenses with minimal tissue manipulation. Measurements of the anterior capsule thickness is reported for the first time in young and old mice from four inbred strains, BALB/c, FVB/N, C57BL/6, and 129X1, and the outbred strain ICR. Our data demonstrates that the mouse anterior lens capsule continues to grow postnatally similar to that described in other mammals. It is also shown there is a significant difference in anterior lens capsule thickness between unrelated mouse strains, suggesting that capsule thickness is a quantitative trait shared by strains with common ancestry. Measurements, taken from other regions of FVB/N capsules revealed the anterior pole to be the thickest, followed by the equatorial region and posterior pole. In addition to mouse, anterior capsule measurements taken from intact cattle, rabbit, rat lenses, and human capsulotomy specimens correlated with the overall size of the animal. Anat Rec, 2008. © 2008 Wiley‐Liss, Inc.
Effect of ace inhibitors and TMOF on growth, development, and trypsin activity of larval Spodoptera littoralis
Authors: Lemeire Els , Borovsky Dov , Van Camp John , Smagghe Guy 
Published: October 2008

AbstractAngiotensin converting enzyme (ACE) is a zinc metallopeptidase capable of cleaving dipeptide or dipeptideamide moieties at the C‐terminal end of peptides. ACE is present in the hemolymph and reproductive tissues of insects. The presence of ACE in the hemolymph and its broad substrate specificity suggests an important role in processing of bioactive peptides. This study reports the effects of ACE inhibitors on larval growth in the cotton leafworm Spodoptera littoralis. Feeding ACE inhibitors ad lib decreased the growth rate, inhibited ACE activity in the larval hemolymph, and down‐regulated trypsin activity in the larval gut. These results indicate that S. littoralis ACE may influence trypsin biosynthesis in the larval gut by interacting with a trypsin‐modulating oostatic factor (TMOF). Injecting third instar larvae with a combination of Aea‐TMOF and the ACE inhibitor captopril, down‐regulated trypsin biosynthesis in the larval gut indicating that an Aea‐TMOF gut receptor analogue could be present. Injecting captopril and enalapril into newly molted fifth instar larvae stopped larval feeding and decreased weight gain. Together, these results indicate that ACE inhibitors are efficacious in stunting larval growth and ACE plays an important role in larval growth and development. Arch Insect Biochem Physiol. 2008. © 2008 Wiley‐Liss, Inc.
Biochemical characterization of rab proteins from Bombyx mori
Authors: Uno Tomohide , Moriwaki Tsubasa , Nakamura Masahiko , Matsubara Mamoru , Yamagata Hiroshi , Kanamaru Kengo , Takagi Michihiro 
Published: October 2008

AbstractThe small GTPases known as Rab proteins are key regulators of membrane trafficking. We used RT‐PCR to isolate cDNA clones of insect‐specific Rab proteins (BRabN1 and BRabN2) showing low homology with known Rab proteins from other animals, from mRNA of Bombyx mori. These 2 Rabs were produced in Escherichia coli and purified. BRabN1 bound [3H]‐GDP and [35S]‐GTPγS with dissociation constants of 0.087 × 10−6 M and 1.02 × 10−6 M, respectively, whereas those of BRabN2 were 0.546 × 10−6 M and 1.02 × 10−6 M, respectively. Binding of [35S]‐GTPγS to BRabN1 and N2 was inhibited by GDP and GTP. The GTP‐hydrolysis activities of BRabN1 and N2 were 154 and 35.5 mmol/min/mole, respectively, and bound [35S]‐GTPγS was exchanged efficiently with GTP. BRabN1 also showed ATPase activity and exchange of [35S]‐GTPγS with ATP. Monoclonal antibodies against BRabN1 and N2 did not recognize any other Rab proteins, and Western blotting using the anti‐BRabN1 antibody revealed a single band in the testis of B. mori. These results suggest that BRabN1 and N2 of B. mori bind GTP, convert from the GTP‐bound state to the GDP‐bound state by intrinsic GTP hydrolysis activity, and return to the GTP‐bound state with the exchange, and that BRabN1 is specifically expressed in testis. Arch. Insect Biochem. Physiol. 2008. © 2008 Wiley‐Liss, Inc.
A new versatile gene‐trap vector for insect transgenics
Authors: Lukacsovich Tamas , Hamada Noriko , Miyazaki Sakura , Kimpara Akiyo , Yamamoto Daisuke 
Published: October 2008

AbstractA new piggyBac‐based gene‐trap vector, pB‐GT1, was constructed. pB‐GT1 contains three marker genes, dsRed, Gal4, and EGFP. dsRed is under the control of the constitutive 3xP3 promoter, which induces dsRed expression wherever the vector is inserted in the host genome. The Gal4 sequence has no promoter but is preceded by the splice acceptor site so that it can be transcribed as a transcript fused with the host exon 5′ to the insertion site. EGFP is driven by the constitutive ie+hr promoter but lacks a poly(A)+ signal sequence, and thus the EGFP expression is detectable only when its transcript is fused with the host exon 3′ downstream of the insertion. By the microinjection of the vector into fertilized eggs, we obtained transgenic Drosophila with a single copy of pB‐GT1, which was inserted into the first intron of the ovo gene. The female flies of this transgenic line are sterile, indicating that the insertion inactivated the ovo gene, generating a new allele of this locus, ovopB‐GT1. RT‐PCR analysis demonstrated that an ovo‐Gal4‐fusion transcript is produced in ovopB‐GT1 flies. The fact that UAS‐EGFP reporter expression was detected in ovopB‐GT1 germ cells in a pattern similar to that reported for wild‐type ovo indicates that functional Gal4 is expressed via pB‐GT1, recapitulating the endogenous expression pattern of the trapped gene. pB‐GT1 is thus useful in insect genomics for the efficient assignment of functions of individual genes. Arch. Insect Biochem. Physiol. 2008. © 2008 Wiley‐Liss, Inc.