scholarly journals Maternal taurine supplementation in the late pregnant rat stimulates postnatal growth and induces obesity and insulin resistance in adult offspring

2007 ◽  
Vol 579 (3) ◽  
pp. 823-833 ◽  
Author(s):  
Karin Hultman ◽  
Camilla Alexanderson ◽  
Louise Mannerås ◽  
Mats Sandberg ◽  
Agneta Holmäng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Postnatal Growth ◽  
Adult Offspring ◽  
Taurine Supplementation ◽  
Pregnant Rat

1774-P: Maternal Apical Periodontitis Promotes Insulin Resistance in Adult Offspring

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1774-P
Author(s):  
THAÍS V. TSOSURA ◽  
FERNANDO Y. CHIBA ◽  
MARIA S. MATTERA ◽  
RENATO F. PEREIRA ◽  
CLÉA A. GARBIN ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Apical Periodontitis ◽  
Adult Offspring

scholarly journals Calcium supplementation reverts central adiposity, leptin, and insulin resistance in adult offspring programed by neonatal nicotine exposure

2011 ◽  
Vol 210 (3) ◽  
pp. 349-359 ◽  
Author(s):  
J L Nobre ◽  
P C Lisboa ◽  
A P Santos-Silva ◽  
N S Lima ◽  
A C Manhães ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Leptin Receptor ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Standard Diet ◽  
Adult Offspring ◽  
Nicotine Exposure ◽  
Central Adiposity ◽  
Metabolism Regulation ◽  
The Metabolic Syndrome

Obesity is a worldwide epidemic. Calcium influences energy metabolism regulation, causing body weight loss. Because maternal nicotine exposure during lactation programs for obesity, hyperleptinemia, insulin resistance (IR), and hypothyroidism, we decided to evaluate the possible effect of dietary calcium supplementation on these endocrine dysfunctions in this experimental model. Osmotic minipumps containing nicotine solution (N: 6 mg/kg per day for 14 days) or saline (C) were s.c. implanted in lactating rats 2 days after giving birth (P2). At P120, N and C offspring were subdivided into four groups: 1) C – standard diet; 2) C with calcium supplementation (CCa, 10 g calcium carbonate/kg rat chow); 3) N – standard diet; and 4) N with calcium supplementation (NCa). Rats were killed at P180. As expected, N offspring showed higher visceral and total body fat, hyperleptinemia, lower hypothalamus leptin receptor (OB-R) content, hyperinsulinemia, and higher IR index. Also, higher tyrosine hydroxylase (TH) expression (+51%), catecholamine content (+37%), and serum 25-hydroxyvitamin D3(+76%) were observed in N offspring. Dietary calcium supplementation reversed adiposity, hyperleptinemia, OB-R underexpression, IR, TH overexpression, and vitamin D. However, this supplementation did not reverse hypothyroidism. In NCa offspring,Sirt1mRNA was lower in visceral fat (−37%) and higher in liver (+42%). In conclusion, dietary calcium supplementation seems to revert most of the metabolic syndrome parameters observed in adult offspring programed by maternal nicotine exposure during lactation. It is conceivable that the reduction in fat massper se, induced by calcium therapy, is the main mechanism that leads to the increment of insulin action.

159 EFFECTS OF EMBRYO TRANSFER IN A LARGER BREED ON POSTNATAL GROWTH AND GLUCOSE METABOLISM IN HORSES

2013 ◽  
Vol 25 (1) ◽  
pp. 228
Author(s):  
P. Peugnet ◽  
A. Tarrade ◽  
C. Sandersen ◽  
M. Dahirel ◽  
D. Guillaume ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Embryo Transfer ◽  
Fetal Growth ◽  
Fasting Glucose ◽  
Plasma Concentrations ◽  
Postnatal Growth ◽  
Glucose Regulation ◽  
Intravenous Glucose ◽  
Glucose Clearance

In equids, the size of the uterus determines fetal intrauterine development, which in turn affects postnatal insulin sensitivity and growth rate. We induced intrauterine growth enhancement through embryo transfer using Pony (P), Saddlebred (S), and Draft (D) horses and studied growth and insulin sensitivity in foals from birth to one year of age. Control pregnancies of S-in-S (n = 14) and P-in-P (n = 10) were obtained by AI. Enhanced fetal growth was obtained by transferring S (S-in-D, n = 7) and P embryos (P-in-D, n = 5) into D mares. From birth to weaning (180 days), each foal was kept with its surrogate P, S, or D dam. At 3, 140, and 380 days, glucose clearance and pancreatic beta cell response to exogenous glucose were assessed with an intravenous glucose tolerance test (IVGTT). At 200 days, the euglycemic-hyperinsulinemic clamp method was used to determine the sensitivity and responsiveness of tissues to exogenous insulin. Plasma T3, T4, and IGF1 were assayed at 3 and 180 days. Data were analysed using one-way ANOVA and Tukey post hoc tests. S-in-S were heavier and taller than P-in-P from birth to 380 days (P < 0.001). Before weaning, plasma concentrations of several hormones involved in growth were lower in S-in-S than P-in-P (at 3 and 180 days, respectively, T3: P = 0.08 and P = 0.02, T4: P < 0.001 and P = 0.06, IGF1: P = 0.04 and P < 0.001). No difference was found in glucose regulation between these groups. In contrast, post-weaning insulin resistance was observed in P-in-P at 200 days (P < 0.001) and confirmed at 380 days where they exhibited slower glucose clearance (P = 0.03) associated with higher fasting glucose (P < 0.001) than S-in-S. Fetal growth was not enhanced in S-in-D with no difference in height and weight at birth. Although S-in-D grew faster from 30 to 140 days, growth rates were not different from S-in-S after weaning, weaning coinciding with lower T3 (P < 0.001) in S-in-D than in S-in-S. Glucose regulation was not different between the two groups, but insulin remains to be assayed at 140 and 380 days. Fetal growth was enhanced in P-in-D: at birth, they were heavier (P = 0.01) and taller (P < 0.001) than P-in-P. Growth of P-in-D was faster until weaning. No more difference, however, was observed between P-in-D and P-in-P at 380 days. Plasma concentrations of T3 (P = 0.03) and those of T4 (P < 0.001) were lower at 3 days and T3 was still lower at 180 days (P < 0.001) in P-in-D compared with P-in-P. Moreover, P-in-D developed early insulin resistance: insulin secretion was higher in P-in-D compared with P-in-P (P = 0.002) after IVGTT at 3 days. At 200 days, however, P-in-D and P-in-P had the same sensitivity to insulin. There was no difference in glucose clearance rates at 380 days, but P-in-D had lower fasting glucose (P < 0.001) than P-in-P. Insulin assays at 140 and 380 days are pending. In conclusion, these data indicate that transfer of a small breed embryo into a large breed mare and subsequent suckling by the recipient mare can enhance fetal and postnatal growth and affect the foal’s glycaemia and sensitivity to insulin at birth and in subsequent months. Ongoing work includes analyses of milk samples and effects on general health.

Maternal apical periodontitis increases insulin resistance and modulates the antioxidant defense system in gastrocnemius muscle of adult offspring

2021 ◽  
Author(s):  
Thaís Verônica Saori Tsosura ◽  
Rodrigo Martins dos Santos ◽  
Antonio Hernandes Chaves Neto ◽  
Fernando Yamamoto Chiba ◽  
Ana Carolina Nascimento Carnevali ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Antioxidant Defense ◽  
Gastrocnemius Muscle ◽  
Antioxidant Defense System ◽  
Apical Periodontitis ◽  
Adult Offspring ◽  
Defense System

scholarly journals C-terminal truncation of Pik3r1 in mice models human lipodystrophic insulin resistance uncoupled from dyslipidemia

2017 ◽  
Author(s):  
Albert Kwok ◽  
Ilona Zvetkova ◽  
Sam Virtue ◽  
Isabel Huang-Doran ◽  
Patsy Tomlinson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Tyrosine Kinases ◽  
Target Genes ◽  
Ex Vivo ◽  
Liver Weight ◽  
Postnatal Growth ◽  
Regulatory Subunit ◽  
Severe Insulin Resistance ◽  
Triglyceride Content ◽  
Short Syndrome

SummaryHeterodimeric class IA phosphatidylinositol-3-kinases (PI3K) transduce signals from many receptor tyrosine kinases including the insulin receptor. PI3K recruitment to phosphotyrosines is mediated by Pik3r1 gene products including the most intensely studied PI3K regulatory subunit, p85α, which also binds and regulates the PIP3 phosphatase Pten, and the lipogenic transcription factor Xbp1. Mutations in human PIK3R1 cause SHORT syndrome, featuring lipodystrophy and severe insulin resistance which, uniquely, are uncoupled from fatty liver and dyslipidemia. We describe a novel mouse model of SHORT syndrome made by knock in of the Pik3r1 Y657X mutation. Homozygous embryos die at E11.5, while heterozygous mice exhibit pre-and postnatal growth impairment with diminished placental vascularity. Adipose tissue accretion on high fat feeding was reduced, however adipocyte size was unchanged and preadipocyte differentiation ex vivo unimpaired. Despite severe insulin resistance, heterozygous mice were hypolipidemic, and plasma adiponectin, liver weight, cholesterol, glycogen and triglyceride content were unchanged. Mild downregulation of lipogenic Srebp1, Srebp2 and Chrebp transcriptional activity but no suppression of Xbp1 target genes was seen after fasting. These findings give new insights into the developmental role of Pik3r1, and establish a model of lipodystrophic insulin resistance dissociated from dyslipidemia as seen in SHORT syndrome.

5220Maternal high-fat diet exaggerates the development of diet-induced insulin resistance in adult offspring by enhancing pyroptosis through augmented gasdermin D-mediated pore formation

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N Wada ◽  
H Yamada ◽  
S Motoyama ◽  
M Saburi ◽  
T Sugimoto ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Pore Formation ◽  
Flow Cytometric Analysis ◽  
Adult Offspring ◽  
High Fat ◽  
Expression Levels ◽  
Caspase 1 ◽  
Flow Cytometric ◽  
Tnf Α

Abstract Background Maternal high-fat diet (HFD) has been shown to promote the development of insulin resistance (IR) in adult offspring; however, the underlying mechanisms remain unclear. Approach and results Eight-week-old female wild-type mice (C57BL/6) were fed a HFD or normal diet (ND) one week prior to mating, and received during pregnancy and lactation. Eight-week-old male offspring of both groups were fed a HFD for 8 weeks. Offspring of HFD-fed dams (O-HFD) showed significantly enhanced IR compared with offspring of ND-fed dams (O-ND). There was no difference in body weight, epidydimal white adipose tissue (eWAT) weight, and cumulative caloric intake between the 2 groups. However, eWAT adipocyte size was significantly increased in O-HFD, accompanied by the abundant crown-like structures. Flow cytometric analysis revealed an increased percentage of M1, but not M2, macrophages. Serum and eWAT concentrations of IL-1β, but not TNF-α, were significantly higher in O-HFD than O-ND (3.7-fold and 2.0-fold, respectively, P<0.05). Treatment with NLRP3 inflammasome inhibitor MCC950 completely abrogated the enhanced IR in O-HFD to a similar extent of that in O-ND, although IR was modestly, but not significantly, ameliorated in O-ND even after MCC950 treatment. Consistent with in vivo findings, in vitro polarization of bone marrow-derived macrophages (BMDMs) did not show any difference in TNF-α mRNA expression after conventional stimulation. In contrast, palmitate acid (PA)-mediated metabolic activation of BMDMs following LPS priming showed a significantly higher concentration of IL-1β in culture supernatants from O-HFD (45%, P<0.05). However, protein expression levels of NLRP-3, ASC, and procaspase-1 after LPS priming were equivalent between the 2 groups. Consistently, intracellular flow cytometric analysis of caspase-1 activity after PA activation did not show any difference, which was compatible with the finding that ex vivo caspase-1 activity of eWAT assessed by fluorescent image of IVIS revealed no difference between the 2 groups. To further examine the mechanism of augmented IL-1β release in BMDM of O-HFD, we examined the cleavage of caspase substrate gasdermin D (GSDMD) and subsequent pore formation. Protein and gene expression levels of GSDM-D after LPS priming were significantly higher in O-HFD (50% and 381%, respectively, P<0.05). At 2 hrs after PA stimulation following LPS priming, cleaved GSDM-D was significantly increased in O-HFD (80%, P<0.01). Consistently, percentage of pore formation assessed by ethidium bromide staining was significantly higher in O-HFD (60%, P<0.05), while LDH release could not be observed. Conclusions Our findings demonstrate that maternal HFD exaggerates diet-induced insulin resistance in adult offspring by enhancing pyroptosis through augmented GSDM-D-mediated pore formation.

scholarly journals Placental Restriction Reduces Insulin Sensitivity and Expression of Insulin Signaling and Glucose Transporter Genes in Skeletal Muscle, But Not Liver, in Young Sheep

Endocrinology ◽  
2012 ◽  
Vol 153 (5) ◽  
pp. 2142-2151 ◽  
Author(s):  
Miles J. De Blasio ◽  
Kathryn L. Gatford ◽  
M. Lyn Harland ◽  
Jeffrey S. Robinson ◽  
Julie A. Owens
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Postnatal Growth ◽  
Whole Body ◽  
Poor Growth ◽  
Hepatic Expression ◽  
Metabolic Genes

Poor growth before birth is associated with impaired insulin sensitivity later in life, increasing the risk of type 2 diabetes. The tissue sites at which insulin resistance first develops after intrauterine growth restriction (IUGR), and its molecular basis, are unclear. We have therefore characterized the effects of placental restriction (PR), a major cause of IUGR, on whole-body insulin sensitivity and expression of molecular determinants of insulin signaling and glucose uptake in skeletal muscle and liver of young lambs. Whole-body insulin sensitivity was measured at 30 d by hyperinsulinaemic euglycaemic clamp and expression of insulin signaling genes (receptors, pathways, and targets) at 43 d in muscle and liver of control (n = 15) and PR (n = 13) lambs. PR reduced size at birth and increased postnatal growth, fasting plasma glucose (+15%, P = 0.004), and insulin (+115%, P = 0.009). PR reduced whole-body insulin sensitivity (−43%, P &lt; 0.001) and skeletal muscle expression of INSR (−36%), IRS1 (−28%), AKT2 (−44%), GLUT4 (−88%), GSK3α (−35%), and GYS1 (−31%) overall (each P &lt; 0.05) and decreased AMPKγ3 expression in females (P = 0.030). PR did not alter hepatic expression of insulin signaling and related genes but increased GLUT2 expression (P = 0.047) in males. Whole-body insulin sensitivity correlated positively with skeletal muscle expression of IRS1, AKT2, HK, AMPKγ2, and AMPKγ3 in PR lambs only (each P &lt; 0.05) but not with hepatic gene expression in control or PR lambs. Onset of insulin resistance after PR and IUGR is accompanied by, and can be accounted for by, reduced expression of insulin signaling and metabolic genes in skeletal muscle but not liver.

Dietary enrichment with alpha-linolenic acid during pregnancy attenuates insulin resistance in adult offspring in mice

2014 ◽  
Vol 120 (3) ◽  
pp. 99-111 ◽  
Author(s):  
K. S. Hollander ◽  
C. Tempel Brami ◽  
F. M. Konikoff ◽  
M. Fainaru ◽  
A. Leikin-Frenkel
Keyword(s):  
Insulin Resistance ◽  
Linolenic Acid ◽  
Adult Offspring ◽  
Alpha Linolenic Acid
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