scholarly journals Maternal Adipose Tissue Expansion, A Missing Link in the Prediction of Birth Weight Centile

2019 ◽  
Vol 105 (3) ◽  
pp. e814-e825 ◽  
Author(s):  
Eleanor M Jarvie ◽  
Frances M Stewart ◽  
Jane E Ramsay ◽  
E Ann Brown ◽  
Barbara J Meyer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Birth Weight ◽  
Cord Blood ◽  
Body Fat ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Placental Weight ◽  
Maternal Body Mass Index ◽  
Model Assessment ◽  
Maternal Body

Abstract Context Maternal body mass index (BMI) is associated with increased birth weight but does not explain all the variance in fetal adiposity. Objective To assess the contribution of maternal body fat distribution to offspring birth weight and adiposity. Design Longitudinal study throughout gestation and at delivery. Setting Women recruited at 12 weeks of gestation and followed up at 26 and 36 weeks. Cord blood was collected at delivery. Patients Pregnant women (n = 45) with BMI 18.0 to 46.3 kg/m2 and healthy pregnancy outcome. Methods Maternal first trimester abdominal subcutaneous and visceral adipose tissue thickness (SAT and VAT) was assessed by ultrasound. Main Outcome Measures Maternal body fat distribution, maternal and cord plasma glucose and lipid concentrations, placental weight, birth weight, and fetal adiposity assessed by cord blood leptin. Results VAT was the only anthropometric measure independently associated with birth weight centile (r2 adjusted 15.8%, P = .002). BMI was associated with trimester 2 and trimesters 1 through 3 area under the curve (AUC) glucose and insulin resistance (Homeostatic Model Assessment). SAT alone predicted trimester 2 lipoprotein lipase (LPL) mass (a marker of adipocyte insulin sensitivity) (11.3%, P = .017). VAT was associated with fetal triglyceride (9.3%, P = .047). Placental weight was the only independent predictor of fetal adiposity (48%, P < .001). Maternal trimester 2 and AUC LPL were inversely associated with fetal adiposity (r = -0.69, P = .001 and r = -0.58, P = .006, respectively). Conclusions Maternal VAT provides additional information to BMI for prediction of birth weight. VAT may be a marker of reduced SAT expansion and increased availability of maternal fatty acids for placental transport.

scholarly journals AKR1C2 and AKR1C3 expression in adipose tissue: association with body fat distribution and regulatory variants

2021 ◽  
pp. 111220
Author(s):  
Giada Ostinelli ◽  
Jinchu Vijay ◽  
Marie-Claude Vohl ◽  
Elin Grundberg ◽  
Andre Tchernof
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Regulatory Variants

Epicardial Adipose Tissue Extent: Relationship With Age, Body Fat Distribution, and Coronaropathy

Obesity ◽  
2008 ◽  
Vol 16 (11) ◽  
pp. 2424-2430 ◽  
Author(s):  
Alina Silaghi ◽  
Marie-Dominique Piercecchi-Marti ◽  
Michel Grino ◽  
Georges Leonetti ◽  
Marie C. Alessi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Epicardial Adipose Tissue ◽  
Fat Distribution ◽  
Body Fat Distribution

scholarly journals Fetal alleles predisposing to metabolically favourable adiposity are associated with higher birth weight

2020 ◽  
Author(s):  
WD Thompson ◽  
RN Beaumont ◽  
A Kuang ◽  
NM Warrington ◽  
Y Ji ◽  
...  
Keyword(s):  
Birth Weight ◽  
Cord Blood ◽  
Body Fat ◽  
Genetic Predisposition ◽  
Genetic Variants ◽  
Fat Distribution ◽  
Genome Wide Association Studies ◽  
Genetic Score ◽  
Maternal Genotype ◽  
Adult Body

AbstractBackgroundHigher birth weight is associated with higher adult body mass index (BMI). If genetic variants can be identified with alleles that predispose to both greater fetal growth and to greater adult adiposity, such shared genetic effects might indicate biological processes important in the early patterning of adiposity. However, variants identified in genome-wide association studies of adult BMI have overall been only weakly associated with birth weight. Genetic variants have recently been identified where one allele is associated with higher adult body fat percentage, but lower risk of metabolic disease, likely due to a favourable body fat distribution. The effect of these adult metabolically favourable adiposity alleles on an individual’s own birth weight is unknown.AimWe aimed to test the effect on birth weight of a fetal genetic predisposition to higher metabolically favourable adult adiposity and to compare this with the effects of a fetal genetic predisposition to higher adult BMI. We also aimed to examine the effects of a genetic predisposition to higher metabolically favourable adult adiposity or BMI on other birth anthropometric traits (length, ponderal index, head circumference and skinfold thickness) and on cord-blood insulin, leptin and adiponectin.MethodsWe used published GWAS data from up to 406,063 individuals to estimate the fetal effects on birth weight of alleles that are robustly associated with higher metabolically favourable adult adiposity or BMI. We additionally used 9,350 mother-child pairs from four cohorts to test the effects of the same alleles on other birth anthropometric traits and cord-blood markers. In all analyses, we adjusted for potential confounding due to the maternal genotype. We used inverse-variance weighted meta-analyses to combine summary data across SNPs.ResultsFetal genetic predisposition to higher metabolically favourable adult adiposity was associated with higher birth weight (10 grams (95% CI: 7 to 13) higher mean birth weight per 1 SD pooled “genetic score”). Fetal genetic predisposition to higher adult BMI was also associated with higher birth weight, but with a smaller magnitude of effect (4 grams (95% CI: 0 to 8) higher mean birth weight per 1 SD pooled “genetic score”) and with higher heterogeneity across SNPs. Effects on other birth anthropometric outcomes were consistent with the effect on birth weight but with wider confidence intervals. There was no strong evidence for an effect on cord-blood markers.ConclusionsSome genetic variants previously linked to adult adiposity influence birth weight. Alleles that predispose to higher metabolically favourable adult adiposity collectively have a stronger effect on birth weight than those predisposing to higher BMI. This suggests that the early accumulation of a metabolically favourable fat distribution might underlie part of the observed association between higher birth weight and higher adult BMI. Larger samples are needed to clarify the effects on other birth anthropometric measures and cord-blood markers.

scholarly journals Circulating betatrophin/ANGPTL8 levels correlate with body fat distribution in individuals with normal glucose tolerance but not those with glucose disorders

2019 ◽  
Author(s):  
Jing Zheng ◽  
Juan Liu ◽  
Beverly S Hong ◽  
Yanbing Li
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Body Fat ◽  
Lower Limb ◽  
Fat Distribution ◽  
Normal Glucose Tolerance ◽  
Body Fat Distribution ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Normal Glucose

Abstract Background: The relationship between betatrophin/ANGPTL8 and obesity has been investigated using body mass index (BMI); however, since BMI reflects overall adiposity rather than body fat distribution, it remains unclear whether fat deposition in different areas of the body affects betatrophin expression. Here, we investigated the correlation between circulating betatrophin levels and body fat distribution in patients with different glucose tolerance. Methods: In 128 participants with impaired glucose tolerance (IGT; n = 64) or normal glucose tolerance (NGT; n = 64), we measured circulating betatrophin levels by enzyme-linked immunosorbent assay and body fat distribution (subcutaneous, visceral, and limb fat) using magnetic resonance imaging (MRI) and a body fat meter. Results: After controlling for age, sex, and BMI, betatrophin was correlated positively with visceral adipose tissue-to-subcutaneous adipose tissue ratio ( VAT/SAT ratio; r = 0.339, p = 0.009) and negatively with body fat ratio (BFR; r = -0.275, p = 0.035), left lower limb fat ratio (LLR; r = -0.330, p = 0.011), and right lower limb fat ratio (RLR; r = -0.288, p = 0.027) in the NGT group, with these correlations remaining after controlling for triglycerides. VAT/SAT ratio (standardized β = 0.419, p = 0.001) was independently associated with serum betatrophin levels; however, betatrophin was not associated with body fat distribution variables in the IGT group. Conclusions: Circulating betatrophin levels correlated positively with VAT/SAT ratio and negatively with lower limb fat, but not subcutaneous or upper limb fat, in individuals with normal glucose tolerance. Thus, betatrophin may be a poten­tial biomarker for body fat distribution in individuals without glucose disorders.

scholarly journals Abdominal adipose tissue: Significance and methods of detection

2005 ◽  
Vol 58 (5-6) ◽  
pp. 258-264 ◽  
Author(s):  
Biljana Srdic ◽  
Edita Stokic ◽  
Agneza Polzovic ◽  
Sinisa Babovic
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Visceral Fat ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Abdominal Adipose Tissue ◽  
Fat Depots ◽  
Advantages And Disadvantages ◽  
Increased Risk ◽  
Menopausal Women

Introduction. The presence of excess fat in the abdomen, out of proportion to total body fat, is associated with increased risk for cardiovascular and metabolic diseases and other complications of obesity. Histoanatomical characteristics of the abdominal adipose tissue In regard to subcutaneous fat, accumulation of visceral abdominal adipose tissue is more associated with increased metabolic risk. However, mean have more visceral fat than pre-menopausal women. Compared with pre-menopausal women, postmenopausal women have 49% more intraabdominal fat, regardless of age and total fat mass. Measurement of abdominal fat depots Various anthropometric indicators have been suggested for measuring body fat distribution. All of them have advantages and disadvantages, in relation to their interpretation and use. Many are specified as ratios and are difficult to interpret biologically, whereas a change in body fat distribution may exhibit little or no change in the ratios. Waist circumference and sagittal abdominal diameter are good predictors of visceral fat. But, extreme individual variations in visceral to subcutaneous ratio demonstrate the limitations of external anthropometry. The best methods to estimate the amount of visceral fat are imaging techniques like computed tomography or magnetic resonance, but they are expensive and inconvinient in routine practice. Conclusion. Further investigations should provide a simple and optimal indicator of abdominal obesity which should correlate with the amount of viscelar fat and the risk. .

scholarly journals MicroRNA-196a links human body fat distribution to adipose tissue extracellular matrix composition

EBioMedicine ◽  
2019 ◽  
Vol 44 ◽  
pp. 467-475 ◽  
Author(s):  
Catriona Hilton ◽  
Matt J. Neville ◽  
Laura B.L. Wittemans ◽  
Marijana Todorcevic ◽  
Katherine E. Pinnick ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adipose Tissue ◽  
Body Fat ◽  
Human Body ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Matrix Composition

Estrogen regulation of adipose tissue lipoprotein lipase—Possible mechanism of body fat distribution

1998 ◽  
Vol 178 (1) ◽  
pp. 101-107 ◽  
Author(s):  
Thomas M. Price ◽  
Susan N. O'Brien ◽  
Brenda H. Welter ◽  
Richard George ◽  
Jyoti Anandjiwala ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Body Fat ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Estrogen Regulation ◽  
Adipose Tissue Lipoprotein Lipase

scholarly journals Phenotypic Heterogeneity in Body Fat Distribution in Patients with Congenital Generalized Lipodystrophy Caused by Mutations in the AGPAT2 or Seipin Genes

2003 ◽  
Vol 88 (11) ◽  
pp. 5433-5437 ◽  
Author(s):  
Vinaya Simha ◽  
Abhimanyu Garg
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Autosomal Recessive ◽  
Acanthosis Nigricans ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Whole Body ◽  
Severe Insulin Resistance ◽  
Congenital Generalized Lipodystrophy ◽  
Chromosome 9Q34

Abstract Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive syndrome characterized by extreme paucity of adipose tissue since birth, acanthosis nigricans, severe insulin resistance, marked hypertriglyceridemia, and early-onset diabetes mellitus. Recently, we reported mutations in the 1-acylglycerol-3-phosphate O-acyltransferase 2 (AGPAT2) gene in CGL pedigrees linked to chromosome 9q34 (CGL1 subtype), and mutations in the Seipin gene were reported in pedigrees linked to chromosome 11q13 (CGL2 subtype). Whether the two subtypes have differences in body fat distribution has not been investigated. We, therefore, compared whole-body adipose tissue distribution by magnetic resonance imaging in 10 CGL patients, of whom seven (six females, one male) had CGL1 and three (two males, one female) had CGL2. Both subtypes had marked lack of metabolically active adipose tissue located at most sc, intermuscular, bone marrow, intraabdominal, and intrathoracic regions. Paucity of mechanical adipose tissue in the palms, soles, orbits, scalp, and periarticular regions was noted in CGL2, whereas it was well preserved in CGL1 patients. We conclude that CGL patients with Seipin mutations have a more severe lack of body fat, which affects both metabolically active and mechanical adipose tissue, compared with patients with mutations in the AGPAT2 gene.

scholarly journals Visceral Adipose Tissue and Metabolic Complications of Obesity Are Reduced in Prader-Willi Syndrome Female Adults: Evidence for Novel Influences on Body Fat Distribution

2001 ◽  
Vol 86 (9) ◽  
pp. 4330-4338 ◽  
Author(s):  
Anthony P. Goldstone ◽  
E. Louise Thomas ◽  
Audrey E. Brynes ◽  
Jimmy D. Bell ◽  
Gary Frost ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
Sex Steroids ◽  
Density Lipoprotein ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Visceral Adiposity ◽  
Prader Willi Syndrome ◽  
Fasting Insulin ◽  
Glucose Ratio

Visceral obesity is detrimental to health, but the mechanisms controlling body fat distribution are not fully understood. In premenopausal adult females (30 nonobese, 14 obese [body mass index> 30kg/m2]), variance in fasting insulin, glucose, insulin/glucose ratio, C-peptide/insulin ratio, triglycerides, and high-density lipoprotein/low-density lipoprotein-cholesterol ratio, were independently influenced by visceral but not total sc or abdominal sc adipose tissue, as measured by whole-body magnetic resonance imaging. Adult females with Prader-Willi syndrome (n = 13) had significantly reduced visceral adiposity, compared with obese controls (visceral/total sc adipose tissue ratio: 0.067 ± 0.017 vs. 0.108 ± 0.021), independent of their total adiposity (P < 0.001), or use of exogenous sex steroids. This is in contrast to that expected by their physical inactivity, hypogonadism, adult GH deficiency, and psychiatric problems. Females with Prader-Willi syndrome not receiving sex steroids (n = 8) had significantly reduced fasting insulin, insulin/glucose ratio, and triglycerides and increased C-peptide/insulin ratio, compared with obese controls, adjusting for total (P < 0.05) but not visceral adiposity (P = 0.3–0.6), supporting their association. The cause of the reduced visceral adiposity in Prader-Willi syndrome may reflect novel hormonal, hypothalamic, and/or genetic influences on body fat distribution.

Sign in / Sign up

Export Citation Format

Share Document