Prenatal tolbutamide treatment alters plasma glucose and insulin concentrations and negatively affects the postnatal performance of chickens

Franssens, Lies; Lesuisse, Jens; Wang, Y.; Ketelaere, Bart De; Willems, Els; Koppenol, Astrid; Guo, Xiaomin; Buyse, Johan; Decuypere, Eddy; Everaert, Nadia

doi:10.1016/j.domaniend.2015.01.004

Cited by 3 publications

(2 citation statements)

References 49 publications

(72 reference statements)

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“…Commercial kits were used to determine plasma triacylglycerol (TG, Sigma-Aldrich, St. Louis, MO, USA), glucose and NEFA (non-esterified fatty acid, Wako Chemicals, Osaka, Japan) levels. Plasma insulin and interleukin-1β (IL-1β) concentrations were determined by a validated commercial ELISA kit (Cat.# 10-1249-01, Uppsala, Sweden, KMC006; Biosource International, Camarillo, CA, USA, respectively) [28,29].…”

Section: Determination Of Plasma Glucose Triacylglycerol Nefa Insulin and Il-1β Concentrationsmentioning

confidence: 99%

Differential Modulation of 25-hydroxycholecalciferol on Innate Immunity of Broiler Breeder Hens

Chou

Lin

et al. 2021

Animals

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Past immunological studies in broilers focused on juveniles within the rapid pre-slaughter growth period and may not reflect adult immune responses, particularly in breeders managed with chronic feed restriction (R). The study aimed to assess innate immune cell functions in respect to R vs. ad libitum (Ad) feed intake in breeder hens with and without dietary 25-hydroxycholecalciferol (25-OH-D3) supplementation. Ad-feed intake consistently suppressed IL-1β secretion, respiratory burst, and cell livability in peripheral heterophils and/or monocytes along the feeding trial from the age of 51 to 68 weeks. Supplemental 25-OH-D3 repressed IL-1β secretion and respiratory burst of both cells mostly in R-hens, but promoted monocyte phagocytosis, chemotaxis, and bacterial killing activity in Ad-hens in accompany with relieved hyperglycemia, hyperlipidemia, and systemic inflammation. Overnight cultures with leukocytes from R-hens confirmed the differential effects of 25-OH-D3 to rescue immune functions altered by glucose and/or palmitic acid exposure. Studies with specific inhibitors further manifested the operative mechanisms via glucolipotoxicity in a cell type- and function-dependent manner. The results concluded no predominant changes between R- vs. Ad-feed intake on leukocyte defense against pathogens despite some differential differences, but supplemental 25-OH-D3 exerts more pronounced effects in Ad-hens.

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Section: Determination Of Plasma Glucose Triacylglycerol Nefa Insulin and Il-1β Concentrationsmentioning

confidence: 99%

Differential Modulation of 25-hydroxycholecalciferol on Innate Immunity of Broiler Breeder Hens

Chou

Lin

et al. 2021

Animals

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“…Plasma insulin levels were determined by a validated commercial ELISA kit (Cat. # 10-1249-01, Uppsala, Sweden) [17].…”

Section: Prandial Changes Of Plasma Insulin and Glucose Levelsmentioning

confidence: 99%

Unrestricted Feed Intake Induces β-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens

Huang

Chang

Chen

et al. 2020

Animals

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Past studies regarding to insulin secretion and glucose disposal in chickens were focused on rapidly growing juvenile broilers and may not reflect glucose/insulin physiology in adulthood. The study aimed to assess insulin secretion and glucose disposal in respect to restricted (R) vs. ad libitum (Ad) feed intake for obesity development in broiler breeder hens. Hens at age of 26 weeks were continued on R rations, or allowed Ad-feed intake up to 45 weeks. Results from prandial changes and glucose tolerance test suggested that Ad-feed intake to 45 weeks impaired insulin secretion and glucose clearance, and, thus, caused hyperglycemia in accompany with transient hyperinsulinemia at age of 33 weeks (p < 0.05). The alterations were shown operating at both transcript and protein level of insulin gene expression per se and at ATP supply for insulin release as evidenced by consistent changes of enzyme expression and activity in pyruvate anaplerosis in the β-islets (p < 0.05). Ad-feed intake also increased β-islet triacylglycerol and ceramide accumulation and provoked interleukin-1β (IL-1β) production (p < 0.05), which were further manifested by a detrimental increase of caspase 3/7 activity and cell apoptosis (p < 0.05). Results support the conclusion that release to Ad-feed intake in broiler breeder hens transiently induced hyperinsulinemia along rapid bodyweight gain and adiposity, but later provoked lipotoxicity and inflammation leading to β-cell apoptosis and ultimately impaired insulin secretion and glucose disposal.

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Obesity-associated cardiac pathogenesis in broiler breeder hens: Development of metabolic cardiomyopathy ,

Chen

Huang

et al. 2017

Poultry Science

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Feed intake is typically restricted (R) in broiler hens to avoid obesity and improve egg production and livability. To determine whether improved heart health contributes to improved livability, fully adult 45-week-old R hens were allowed to consume feed to appetite (ad libitum; AL) up to 10 wk (70 d). Mortality, contractile functions, and morphology at 70 d, and measurements of cardiac hypertrophic remodeling at 7 d and 21 d were made and compared between R and AL hens. Outcomes for cardiac electrophysiology and mortality, reported separately, found increased mortality in AL hens in association with cardiac pathological hypertrophy and contractile dysfunction. The present study aimed to delineate metabolic cardiomyopathies underlying the etiology of obesity-associated cardiac pathology. Metabolic measurements were made in hens continued on R rations or assigned to AL feeding after 7 d and 21 days. AL feeding increased plasma insulin, glucose, and non-esterified fatty acid (NEFA) concentrations by 21 d (P < 0.05). Metabolic cardiomyopathy in AL-hens was confirmed by cardiac triacylglycerol (TG) and ceramide accumulation consistent with up-regulation of related enzyme gene expressions, and by increased indices of oxidation stress (P < 0.05). In contrast to R hens, cardiac pyruvate dehydrogenase (PDH) activity and glucose transporter (GLUT) gene expressions increased progressively while carnitine palmitoyltransferase-1 (CPT-1) transcript levels in AL hens declined from 7 d to 21 d (P < 0.05), reflecting a shift from an oxidative to a more glycolytic metabolism, a typical metabolic derangement associated with cardiac hypertrophic remodeling. Cardiac pathogenesis in AL hens was further indicated by increased leukocyte infiltrates, interleukin-1β (IL-1β) and IL-6 production, cellular apoptosis, interstitial fibrosis, and expression of the heart failure marker myosin heavy chain (MHC-β; cardiac muscle beta) (P < 0.05). Results support the conclusion that diabetic conditions, cardiac inflammation and lipotoxic metabolic derangements act as pathological cues to trigger pathogenic changes along cardiac hypertrophy in AL hens.

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Prenatal tolbutamide treatment alters plasma glucose and insulin concentrations and negatively affects the postnatal performance of chickens

Cited by 3 publications

References 49 publications

Differential Modulation of 25-hydroxycholecalciferol on Innate Immunity of Broiler Breeder Hens

Differential Modulation of 25-hydroxycholecalciferol on Innate Immunity of Broiler Breeder Hens

Unrestricted Feed Intake Induces β-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens

Obesity-associated cardiac pathogenesis in broiler breeder hens: Development of metabolic cardiomyopathy ,

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