Impaired glucose homeostasis during postimplantation pregnancy in the mouse following acute exposure to ethanol, with particular reference to the uterus and embryo

Murdoch, R. N.; Simm, Brett

doi:10.1016/0885-4505(92)90008-m

Cited by 5 publications

(3 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ethanol induces a variety of pathophysiological changes in the uterus in non-pregnant as well as pregnant laboratory animals, including alterations in the methylation of membrane phospholipids, increased oxygen tension, impaired glucose homeostasis, altered spontaneous motility, prostaglandin production, triglyceride metabolism and tissue atrophy (Murdoch and Edwards, 1992;Mitchell and Van Kainen, 1992;Murdoch and Simm, 1992;Chaud et ah, 1991;Murdoch, 1987). Many of these changes are believed to be indirect.…”

Section: Resultsmentioning

confidence: 99%

“…However, comparing the 169 genes shared between bone and liver reveals only 66 that were regulated in the same direction, which suggests activation of different signaling pathways. This conclusion is further supported by the observation that of 5531 genes assayed, only one was altered by alcohol in all 3 organs and the direction of change of this gene differed between bone and the other two organs.DISCUSSION 09/06/00 Page 6Ethanol induces a variety of pathophysiological changes in the uterus in non-pregnant as well as pregnant laboratory animals, including alterations in the methylation of membrane phospholipids, increased oxygen tension, impaired glucose homeostasis, altered spontaneous motility, prostaglandin production, triglyceride metabolism and tissue atrophy (Murdoch and Edwards, 1992;Mitchell and Van Kainen, 1992;Murdoch and Simm, 1992; Chaud et ah, 1991;Murdoch, 1987). Many of these changes are believed to be indirect.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Alcohol and Adaptation to Mechanical Usage

Turner¹

2000

View full text Add to dashboard Cite

Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget, Paperwork Reduction Project (0704-0188), Washington, DC 20503 AGENCY USE ONLY (Leave blank) REPORT DATE October 2000 REPORT TYPE AND DATES COVEREDAnnual (1 Sep 99 -31 Aug 00) TITLE AND SUBTITLE Alcohol and Adaptation to Mechanical Usage AUTHOR(S)Russell T. Turner, Ph.D. FUNDING NUMBERS DAMD17-98-1-8517 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)Mayo Foundation Rochester, Minnesota 55905 E-MAIL: rolbiecki.lori@mayo.edu These studies are designed to determine whether ethanol antagonizes the ability of the skeleton to adapt to increased mechanical usage. Ethanol reversibly alters the biophysical properties of cell membranes.The overall hypothesis to be tested in adult rats is that these membrane changes disrupt essential cell signaling pathways for one or more cytokines, growth factors and polypeptide hormones that regulate bone modeling and remodeling.This report summarizes our progress from 01 September 1999 to 31 August 2000. During Year 2 of the award we have continued analysis of experiments performed in Year 1 related to Tasks 1-4 and 8.Additional experiments were performed to accomplish Task 8. Progress was also made on Tasks 6, 7, and 8.The new studies are directed toward determination of the effects of ethanol on: the skeletal readaptation to normal weight bearing following unloading (Task 6), skeletal adaptation to treadmill running (Task 7), PTH-induced increases in mRNA levels for bone matrix proteins (Task 8), and PTH-induced increases in osteoblast number and bone formation (Task 9). SUBJECT TERMS Neurotoxin NUMBER OF PAGES INTRODUCTIONChronic alcohol abuse is an important risk factor for osteoporosis. The ultimate goal of this research is to identify the cellular and molecular mechanisms responsible for mediating ethanol's dose-and time-dependent actions on bone turnover, mass, architecture, and strength. It is well established that ethanol reversibly alters the biophysical properties of cell membranes and in doing so disturbs normal membrane function. The proposed studies in young adult rats will test our working hypothesis that these membrane changes disrupt essential cell signaling pathways for one or more bone cells "coupling" factors and/or polypeptide hormones that regulate bone modeling and remodeling. These changes are postulated to lead to the bone loss associated with chronic alcohol abuse. If our hypothesis is correct, then ethanol antagonizes the ability of t...

show abstract

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Alcohol and Adaptation to Mechanical Usage

Turner¹

2000

View full text Add to dashboard Cite

show abstract

“…Maternal plasma glucose levels, blood glucose turnover, and placental glucose uptake are all decreased in rats exposed to alcohol either before or during pregnancy. [21][22][23][24][25][26] Similarly, prenatal alcohol exposure (PAE) reduces glucose levels in fetal blood 23,24 and brain, 25,26 reduces fetal glucose consumption and utilization, 27,28 reduces fetal hepatic glycogen content, 24 and increases fetal plasma ketones. 24 Overall, these studies suggest that alcohol reduces maternal-fetal glucose availability but do not provide a mechanistic understanding of such changes or their consequences to fetal development.…”

Section: Introductionmentioning

confidence: 99%

Alcohol blunts pregnancy‐mediated insulin resistance and reduces fetal brain glucose despite elevated fetal gluconeogenesis, and these changes associate with fetal weight outcomes

Saini,

Mooney,

Smith

2023

The FASEB Journal

View full text Add to dashboard Cite

Prenatal alcohol exposure (PAE) impairs fetal growth and neurodevelopment. Although alcohol is well known to alter metabolism, its impact on these processes during pregnancy is largely unexplored. Here, we investigate how alcohol affects maternal–fetal glucose metabolism using our established mouse binge model of PAE. In the dam, alcohol reduces the hepatic abundance of glucose and glycolytic intermediates, and the gluconeogenic enzymes glucose‐6‐phosphtase and phosphoenolpyruvate carboxykinase. Fasting blood glucose is also reduced. In a healthy pregnancy, elevated maternal gluconeogenesis and insulin resistance ensures glucose availability for the fetus. Glucose and insulin tolerance tests reveal that alcohol impairs the dam's ability to acquire insulin resistance. Alcohol‐exposed dams have enhanced glucose clearance (p < .05) in early gestation, after just two days of alcohol, and this persists through late term when fetal glucose needs are maximal. However, maternal plasma insulin levels, hepatic insulin signaling, and the abundance of glucose transporter proteins remain unchanged. In the PAE fetus, the expression of hepatic gluconeogenic genes is elevated, and there is a trend for elevated blood and liver glucose levels. In contrast, fetal brain and placental glucose levels remain low. This reduced maternal fasting glucose, reduced hepatic glucose, and elevated glucose clearance inversely correlated with fetal body and brain weight. Taken together, these data suggest that alcohol blunts the adaptive changes in maternal glucose metabolism that otherwise enhance fetal glucose availability. Compensatory attempts by the fetus to increase glucose pools via gluconeogenesis do not normalize brain glucose. These metabolic changes may contribute to the impaired fetal growth and brain development that typifies PAE.

show abstract