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Article ; Online: Comparative lipidome study of maternal plasma, milk, and lamb plasma in sheep.

Thangaraj, Soundara Viveka / Ghnenis, Adel / Pallas, Brooke / Vyas, Arpita Kalla / Gregg, Brigid / Padmanabhan, Vasantha

Scientific reports

2024 Volume 14, Issue 1, Page(s) 7401

Abstract: Lipids play a critical role in neonate development and breastmilk is the newborn's major source of lipids. Milk lipids directly influence the neonate plasma lipid profile. The milk lipidome is dynamic, influenced by maternal factors and related to the ... ...

Abstract	Lipids play a critical role in neonate development and breastmilk is the newborn's major source of lipids. Milk lipids directly influence the neonate plasma lipid profile. The milk lipidome is dynamic, influenced by maternal factors and related to the maternal plasma lipidome. The close inter-relationship between the maternal plasma, milk and neonate plasma lipidomes is critical to understanding maternal-child health and nutrition. In this exploratory study, lipidomes of blood and breast milk from Suffolk sheep and matched lamb blood (n = 13), were profiled on day 34 post birth by untargeted mass spectrometry. Comparative multivariate analysis of the three matrices identified distinct differences in lipids and class of lipids amongst them. Paired analysis identified 346 differential lipids (DL) and 31 correlated lipids (CL) in maternal plasma and milk, 340 DL and 32 CL in lamb plasma and milk and 295 DL and 16 CL in maternal plasma and lamb plasma. Conversion of phosphatidic acid to phosphatidyl inositol was the most active pathway in lamb plasma compared to maternal plasma. This exploratory study illustrates the partitioning of lipids across maternal plasma, milk and lamb plasma and the dynamic relationship between them, reiterating the need to study these three matrices as one biological system.
MeSH term(s)	Female ; Animals ; Sheep ; Humans ; Milk/metabolism ; Lipidomics ; Milk, Human/metabolism ; Nutritional Status ; Plasma ; Lipids
Chemical Substances	Lipids
Language	English
Publishing date	2024-03-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-58116-5
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Article ; Online: Gestational testosterone excess early to mid-pregnancy disrupts maternal lipid homeostasis and activates biosynthesis of phosphoinositides and phosphatidylethanolamines in sheep.

Saadat, Nadia / Pallas, Brooke / Ciarelli, Joseph / Vyas, Arpita Kalla / Padmanabhan, Vasantha

Scientific reports

2024 Volume 14, Issue 1, Page(s) 6230

Abstract: Gestational hyperandrogenism is a risk factor for adverse maternal and offspring outcomes with effects likely mediated in part via disruptions in maternal lipid homeostasis. Using a translationally relevant sheep model of gestational testosterone (T) ... ...

Abstract	Gestational hyperandrogenism is a risk factor for adverse maternal and offspring outcomes with effects likely mediated in part via disruptions in maternal lipid homeostasis. Using a translationally relevant sheep model of gestational testosterone (T) excess that manifests maternal hyperinsulinemia, intrauterine growth restriction (IUGR), and adverse offspring cardiometabolic outcomes, we tested if gestational T excess disrupts maternal lipidome. Dimensionality reduction models following shotgun lipidomics of gestational day 127.1 ± 5.3 (term 147 days) plasma revealed clear differences between control and T-treated sheep. Lipid signatures of gestational T-treated sheep included higher phosphoinositides (PI 36:2, 39:4) and lower acylcarnitines (CAR 16:0, 18:0, 18:1), phosphatidylcholines (PC 38:4, 40:5) and fatty acids (linoleic, arachidonic, Oleic). Gestational T excess activated phosphatidylethanolamines (PE) and PI biosynthesis. The reduction in key fatty acids may underlie IUGR and activated PI for the maternal hyperinsulinemia evidenced in this model. Maternal circulatory lipids contributing to adverse cardiometabolic outcomes are modifiable by dietary interventions.
MeSH term(s)	Pregnancy ; Female ; Sheep ; Animals ; Phosphatidylethanolamines ; Hyperandrogenism ; Phosphatidylinositols ; Testosterone ; Fatty Acids ; Homeostasis ; Hyperinsulinism ; Cardiovascular Diseases
Chemical Substances	Phosphatidylethanolamines ; Phosphatidylinositols ; Testosterone (3XMK78S47O) ; Fatty Acids
Language	English
Publishing date	2024-03-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-56886-6
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Article ; Online: Impact of maternal substance use on offspring's cardiovascular health.

Janardhan, Nitya / Roy, Pritha Ghosh / Vyas, Arpita Kalla

Toxicology and applied pharmacology

2022 Volume 450, Page(s) 116164

Abstract: Substance use (SU) during pregnancy is on the rise, posing significant risks to the developing fetus. The adverse impact of maternal alcohol and nicotine use during the perinatal period on offspring health has been well established, including their ... ...

Abstract	Substance use (SU) during pregnancy is on the rise, posing significant risks to the developing fetus. The adverse impact of maternal alcohol and nicotine use during the perinatal period on offspring health has been well established, including their associations with adverse cardiovascular health in offspring. However, limited studies examine the impact of other well-known SU utilized during pregnancy on offspring's cardiovascular health. This review summarizes the proposed mechanism of action of four commonly utilized substances: cocaine, marijuana, methamphetamine, and opioids, and their cardiovascular impact. Furthermore, we will review the current understanding of the adverse impact of substance use during pregnancy on offspring's cardiovascular system based on existing studies. This review will also highlight possible molecular mechanisms underlying the in-utero adverse programming of offspring's cardiovascular system secondary to SU in pregnancy and address the gaps in current understanding of how SU adversely impacts the developing cardiovascular system of offspring in utero.
MeSH term(s)	Female ; Heart ; Humans ; Pregnancy ; Prenatal Exposure Delayed Effects ; Substance-Related Disorders/epidemiology
Language	English
Publishing date	2022-07-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2022.116164
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Article ; Online: Developmental programming: An exploratory analysis of pancreatic islet compromise in female sheep resulting from gestational BPA exposure.

Ciarelli, Joseph / Thangaraj, Soundara Viveka / Sun, Haijing / Domke, Stephanie / Alkhatib, Bashar / Vyas, Arpita Kalla / Gregg, Brigid / Sargis, Robert M / Padmanabhan, Vasantha

Molecular and cellular endocrinology

2024 Volume 588, Page(s) 112202

Abstract: Developmental exposure to endocrine disruptors like bisphenol A (BPA) are implicated in later-life metabolic dysfunction. Leveraging a unique sheep model of developmental programming, we conducted an exploratory analysis of the programming effects of BPA ...

Abstract	Developmental exposure to endocrine disruptors like bisphenol A (BPA) are implicated in later-life metabolic dysfunction. Leveraging a unique sheep model of developmental programming, we conducted an exploratory analysis of the programming effects of BPA on the endocrine pancreas. Pregnant ewes were administered environmentally relevant doses of BPA during gestational days (GD) 30-90, and pancreata from female fetuses and adult offspring were analyzed. Prenatal BPA exposure induced a trend toward decreased islet insulin staining and β-cell count, increased glucagon staining and α-cell count, and increased α-cell/β-cell ratio. Findings were most consistent in fetal pancreata assessed at GD90 and in adult offspring exposed to the lowest BPA dose. While not assessed in fetuses, adult islet fibrosis was increased. Collectively, these data provide further evidence that early-life BPA exposure is a likely threat to human metabolic health. Future studies should corroborate these findings and decipher the molecular mechanisms of BPA's developmental endocrine toxicity.
MeSH term(s)	Animals ; Benzhydryl Compounds/toxicity ; Female ; Phenols/toxicity ; Pregnancy ; Sheep ; Prenatal Exposure Delayed Effects/chemically induced ; Prenatal Exposure Delayed Effects/pathology ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Islets of Langerhans/pathology ; Endocrine Disruptors/toxicity ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Maternal Exposure/adverse effects ; Insulin/metabolism ; Fetus/drug effects ; Glucagon-Secreting Cells/drug effects ; Glucagon-Secreting Cells/metabolism ; Glucagon-Secreting Cells/pathology
Chemical Substances	Benzhydryl Compounds ; bisphenol A (MLT3645I99) ; Phenols ; Endocrine Disruptors ; Insulin
Language	English
Publishing date	2024-03-27
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2024.112202
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Article ; Online: Sex-Specific Perturbation of Systemic Lipidomic Profile in Newborn Lambs Impacted by Prenatal Testosterone Excess.

Saadat, Nadia / Ciarelli, Joseph / Pallas, Brooke / Padmanabhan, Vasantha / Vyas, Arpita Kalla

Endocrinology

2023 Volume 165, Issue 2

Abstract: Gestational hyperandrogenism adversely impacts offspring health. Using an ovine model, we found that prenatal testosterone (T) excess adversely affects growth and cardiometabolic outcomes in female offspring and produces sex-specific effects on fetal ... ...

Abstract	Gestational hyperandrogenism adversely impacts offspring health. Using an ovine model, we found that prenatal testosterone (T) excess adversely affects growth and cardiometabolic outcomes in female offspring and produces sex-specific effects on fetal myocardium. Since lipids are essential to cardiometabolic function, we hypothesized that prenatal T excess leads to sex-specific disruptions in lipid metabolism at birth. Shotgun lipidomics was performed on the plasma samples collected 48 hours after birth from female (F) and male (M) lambs of control (C) and (T) sheep (CF = 4, TF = 7, CM = 5, TM = 10) and data were analyzed by univariate analysis, multivariate dimensionality reduction modeling followed by functional enrichment, and pathway analyses. Biosynthesis of phosphatidylserine was the major pathway responsible for sex differences in controls. Unsupervised and supervised models showed separation between C and T in both sexes with glycerophospholipids and glycerolipids classes being responsible for the sex differences between C and T. T excess increased cholesterol in females while decreasing phosphatidylcholine levels in male lambs. Specifically, T excess: 1) suppressed the phosphatidylethanolamine N-methyltransferase (PEMT) phosphatidylcholine synthesis pathway overall and in TM lambs as opposed to suppression of carnitine levels overall and TF lambs; and 2) activated biosynthesis of ether-linked (O-)phosphatidylethanolamine and O-phosphatidylcholine from O-diacylglycerol overall and in TF lambs. Higher cholesterol levels could underlie adverse cardiometabolic outcomes in TF lambs, whereas suppressed PEMT pathway in TM lambs could lead to endoplasmic reticulum stress and defective lipid transport. These novel findings point to sex-specific effects of prenatal T excess on lipid metabolism in newborn lambs, a precocial ovine model of translational relevance.
MeSH term(s)	Pregnancy ; Animals ; Sheep ; Female ; Male ; Animals, Newborn ; Hyperandrogenism ; Lipidomics ; Testosterone/pharmacology ; Cardiovascular Diseases ; Phosphatidylcholines ; Cholesterol
Chemical Substances	Testosterone (3XMK78S47O) ; Phosphatidylcholines ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2023-12-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqad187
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Article ; Online: Impact of Adverse Gestational Milieu on Maternal Cardiovascular Health.

Alkhatib, Bashar / Salimi, Shadi / Jabari, Mary / Padmanabhan, Vasantha / Vyas, Arpita Kalla

Endocrinology

2023 Volume 164, Issue 6

Abstract: Cardiovascular disease affects 1% to 4% of the nearly 4 million pregnancies in the United States each year and is the primary cause of pregnancy-related mortality. Adverse pregnancy outcomes are associated with cardiovascular complications during ... ...

Abstract	Cardiovascular disease affects 1% to 4% of the nearly 4 million pregnancies in the United States each year and is the primary cause of pregnancy-related mortality. Adverse pregnancy outcomes are associated with cardiovascular complications during pregnancy persisting into the postpartum period. Recently, investigations have identified an altered sex hormone milieu, such as in the case of hyperandrogenism, as a causative factor in the development of gestational cardiovascular dysfunction. The mechanisms involved in the development of cardiovascular disease in postpartum women are largely unknown. Animal studies have attempted to recapitulate adverse pregnancy outcomes to investigate causal relationships and molecular underpinnings of adverse gestational cardiac events and progression to the development of cardiovascular disease postpartum. This review will focus on summarizing clinical and animal studies detailing the impact of adverse pregnancy outcomes, including preeclampsia, gestational diabetes mellitus, and maternal obesity, on gestational cardiometabolic dysfunction and postpartum cardiovascular disease. Specifically, we will highlight the adverse impact of gestational hyperandrogenism and its potential to serve as a biomarker for maternal gestational and postpartum cardiovascular dysfunctions.
MeSH term(s)	Pregnancy ; Female ; Humans ; Cardiovascular Diseases/etiology ; Hyperandrogenism/complications ; Pregnancy Outcome ; Diabetes, Gestational ; Postpartum Period
Language	English
Publishing date	2023-04-12
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqad060
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Article ; Online: Case of hypercalcemia secondary to hypervitaminosis a in a 6-year-old boy with autism.

Vyas, Arpita Kalla / White, Neil H

Case reports in endocrinology

2011 Volume 2011, Page(s) 424712

Abstract: Vitamin A intoxication secondary to over-the-counter nutritional supplements and from its use in acne treatment has been described. However, there have been very few case reports of chronic hypervitaminosis A leading to hypercalcemia in the pediatric ... ...

Abstract	Vitamin A intoxication secondary to over-the-counter nutritional supplements and from its use in acne treatment has been described. However, there have been very few case reports of chronic hypervitaminosis A leading to hypercalcemia in the pediatric population. This paper describes a boy with hypercalcemia secondary to chronic vitamin A intoxication in the context of vitamin A usage for therapy of autism. In addition to discontinuation of vitamin A, hyperhydration, and furosemide, the hypercalcemia in this patient required the use of prednisone and pamidronate to normalize the calcium.
Language	English
Publishing date	2011-09-11
Publishing country	United States
Document type	Case Reports
ZDB-ID	2627633-1
ISSN	2090-651X ; 2090-6501
ISSN (online)	2090-651X
ISSN	2090-6501
DOI	10.1155/2011/424712
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Article ; Online: Reclassifying inflammatory bowel disease with capsule endoscopy in children.

Joshi, Shruti Shree / Vyas, Arpita Kalla / Vyas, Dinesh / Kalla, Rahul

Jornal de pediatria

2013 Volume 89, Issue 5, Page(s) 514–515

MeSH term(s)	Capsule Endoscopy/methods ; Female ; Humans ; Inflammatory Bowel Diseases/pathology ; Intestine, Small/pathology ; Male
Language	English
Publishing date	2013-07-12
Publishing country	Brazil
Document type	Letter ; Comment
ZDB-ID	731324-x
ISSN	1678-4782 ; 0021-7557
ISSN (online)	1678-4782
ISSN	0021-7557
DOI	10.1016/j.jped.2013.07.002
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Article ; Online: Developmental programming: Sex-specific programming of growth upon prenatal bisphenol A exposure.

Vyas, Arpita Kalla / Veiga-Lopez, Almudena / Ye, Wen / Abi Salloum, Bachir / Abbott, David H / Yang, Shengping / Liao, Chunyang / Kannan, Kurunthachalam / Padmanabhan, Vasantha

Journal of applied toxicology : JAT

2019 Volume 39, Issue 11, Page(s) 1516–1531

Abstract: In both human and animals, in utero exposure to bisphenol A (BPA), an endocrine-disrupting chemical used in the production of plastics and epoxy resins, has been shown to affect offspring reproductive and metabolic health during adult life. We ... ...

Abstract	In both human and animals, in utero exposure to bisphenol A (BPA), an endocrine-disrupting chemical used in the production of plastics and epoxy resins, has been shown to affect offspring reproductive and metabolic health during adult life. We hypothesized that the effect of prenatal exposure to environmentally relevant doses of BPA will be evident during fetal organogenesis and fetal/postnatal growth trajectory. Pregnant ewes were administered BPA subcutaneously from 30 to 90 days of gestation (term 147 days). Fetal organ weight, anthropometric measures, maternal/fetal hormones and postnatal growth trajectory were measured in both sexes. Gestational BPA administration resulted in higher accumulation in male than female fetuses only at fetal day 65, with minimal impact on fetal/maternal steroid milieu in both sexes at both time points. BPA-treated male fetuses were heavier than BPA-treated female fetuses at fetal day 90 whereas this sex difference was not evident in the control group. At the organ level, liver weight was reduced in prenatal BPA-treated female fetuses, while heart and thyroid gland weights were increased in BPA-treated male fetuses relative to their sex-matched control groups. Prenatal BPA treatment also altered the postnatal growth trajectory in a sex-specific manner. Males grew slower during the early postnatal period and caught up later. Females, in contrast, demonstrated the opposite growth trend. Prenatal BPA-induced changes in fetal organ differentiation and early life growth strongly implicate translational relevance of in utero contributions to reproductive and metabolic defects previously reported in adult female offspring.
MeSH term(s)	Animals ; Benzhydryl Compounds/toxicity ; Endocrine Disruptors/toxicity ; Female ; Fetal Development/drug effects ; Male ; Organogenesis/drug effects ; Phenols/toxicity ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Sex Characteristics ; Sheep
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Phenols ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2019-07-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604625-3
ISSN	1099-1263 ; 0260-437X
ISSN (online)	1099-1263
ISSN	0260-437X
DOI	10.1002/jat.3836
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Article ; Online: Effects of the HIV protease inhibitor ritonavir on GLUT4 knock-out mice.

Vyas, Arpita Kalla / Koster, Joseph C / Tzekov, Anatoly / Hruz, Paul W

The Journal of biological chemistry

2010 Volume 285, Issue 47, Page(s) 36395–36400

Abstract: HIV protease inhibitors acutely block glucose transporters (GLUTs) in vitro, and this may contribute to altered glucose homeostasis in vivo. However, several GLUT-independent mechanisms have been postulated. To determine the contribution of GLUT blockade ...

Abstract	HIV protease inhibitors acutely block glucose transporters (GLUTs) in vitro, and this may contribute to altered glucose homeostasis in vivo. However, several GLUT-independent mechanisms have been postulated. To determine the contribution of GLUT blockade to protease inhibitor-mediated glucose dysregulation, the effects of ritonavir were investigated in mice lacking the insulin-sensitive glucose transporter GLUT4 (G4KO). G4KO and control C57BL/6J mice were administered ritonavir or vehicle at the start of an intraperitoneal glucose tolerance test and during hyperinsulinemic-euglycemic clamps. G4KO mice exhibited elevated fasting blood glucose compared with C57BL/6J mice. Ritonavir impaired glucose tolerance in control mice but did not exacerbate glucose intolerance in G4KO mice. Similarly, ritonavir reduced peripheral insulin sensitivity in control mice but not in G4KO mice. Serum insulin levels were reduced in vivo in ritonavir-treated mice. Ritonavir reduced serum leptin levels in C57BL/6J mice but had no effect on serum adiponectin. No change in these adipokines was observed following ritonavir treatment of G4KO mice. These data confirm that a primary effect of ritonavir on peripheral glucose disposal is mediated through direct inhibition of GLUT4 activity in vivo. The ability of GLUT4 blockade to contribute to derangements in the other molecular pathways that influence insulin sensitivity remains to be determined.
MeSH term(s)	Adipokines/metabolism ; Adipose Tissue/cytology ; Adipose Tissue/drug effects ; Adipose Tissue/metabolism ; Animals ; Blood Glucose/metabolism ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay ; Female ; Glucose Intolerance ; Glucose Tolerance Test ; Glucose Transporter Type 4/physiology ; HIV Protease Inhibitors/pharmacology ; Insulin/metabolism ; Insulin Resistance ; Leptin/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal/cytology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Ritonavir/pharmacology
Chemical Substances	Adipokines ; Blood Glucose ; Glucose Transporter Type 4 ; HIV Protease Inhibitors ; Insulin ; Leptin ; Slc2a4 protein, mouse ; Ritonavir (O3J8G9O825)
Language	English
Publishing date	2010-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M110.176321
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