Maternal diabetes in rats. II. Effects on fetal growth and protein turnover

Canavan, J. P.; Goldspink, David F.

doi:10.2337/diabetes.37.12.1671

Cited by 21 publications

(8 citation statements)

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“…The body weight of rats in the O‐DR group was significantly lower compared with those in the O‐CR group. This result agrees with previous reports showing that maternal diabetes induced by STZ produces a decrease in offspring weight (Grill et al ., ; Holemans et al ., ; Porto et al ., ; Ramos‐Alves et al ., ) that has been associated with reduced protein synthesis (Canavan and Goldspink, ). However, several studies have found no changes or even increases in the body weight of the offspring of rats subjected to this experimental procedure (Rocha et al ., ; Nehiri et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Alterations in perivascular innervation function in mesenteric arteries from offspring of diabetic rats

Queiroz

Sastre

Caracuel

et al. 2015

British J Pharmacology

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BACKGROUND AND PURPOSEWe have reported that exposure to a diabetic intrauterine environment during pregnancy increases blood pressure in adult offspring, but the mechanisms involved are not completely understood. This study was designed to analyse a possible role of perivascular sympathetic and nitrergic innervation in the superior mesenteric artery (SMA) in this effect. EXPERIMENTAL APPROACHDiabetes was induced in pregnant Wistar rats by a single injection of streptozotocin. Endothelium-denuded vascular rings from the offspring of control (O-CR) and diabetic rats (O-DR) were used. Vasomotor responses to electrical field stimulation (EFS), NA and the NO donor DEA-NO were studied. The expressions of neuronal NOS (nNOS) and phospho-nNOS (P-nNOS) and release of NA, ATP and NO were determined. Sympathetic and nitrergic nerve densities were analysed by immunofluorescence. KEY RESULTSBlood pressure was higher in O-DR animals. EFS-induced vasoconstriction was greater in O-DR animals. This response was decreased by phentolamine more in O-DR animals than their controls. L-NAME increased EFS-induced vasoconstriction more strongly in O-DR than in O-CR segments. Vasomotor responses to NA or DEA-NO were not modified. NA, ATP and NO release was increased in segments from O-DR. nNOS expression was not modified, whereas P-nNOS expression was increased in O-DR. Sympathetic and nitrergic nerve densities were similar in both experimental groups. CONCLUSIONS AND IMPLICATIONSThe activity of sympathetic and nitrergic innervation is increased in SMA from O-DR animals. The net effect is an increase in EFS-induced contractions in these animals. These effects may contribute to the increased blood pressure observed in the offspring of diabetic rats.

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Section: Discussionmentioning

confidence: 99%

Alterations in perivascular innervation function in mesenteric arteries from offspring of diabetic rats

Queiroz

Sastre

Caracuel

et al. 2015

British J Pharmacology

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“…The experimental induction of diabetes using streptozotocin (STZ) has dosedependent effects: low doses of STZ result in mild gestational diabetes associated with fetal macrosomia (2,4,215,373), whereas high doses induce insulin-deficient diabetes associated with fetal growth restriction (4,64,214,215,359).…”

Section: Maternal Diabetes Fetal Growth and Pancreatic Development mentioning

confidence: 99%

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

McMillen

Robinson²

2005

Physiological Reviews

1,689

1,352

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The "fetal" or "early" origins of adult disease hypothesis was originally put forward by David Barker and colleagues and stated that environmental factors, particularly nutrition, act in early life to program the risks for adverse health outcomes in adult life. This hypothesis has been supported by a worldwide series of epidemiological studies that have provided evidence for the association between the perturbation of the early nutritional environment and the major risk factors (hypertension, insulin resistance, and obesity) for cardiovascular disease, diabetes, and the metabolic syndrome in adult life. It is also clear from experimental studies that a range of molecular, cellular, metabolic, neuroendocrine, and physiological adaptations to changes in the early nutritional environment result in a permanent alteration of the developmental pattern of cellular proliferation and differentiation in key tissue and organ systems that result in pathological consequences in adult life. This review focuses on those experimental studies that have investigated the critical windows during which perturbations of the intrauterine environment have major effects, the nature of the epigenetic, structural, and functional adaptive responses which result in a permanent programming of cardiovascular and metabolic function, and the role of the interaction between the pre- and postnatal environment in determining final health outcomes.

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“…Beta cell exhaustion results in fetal hypoinsulinaemia, which in conjunction with a reduced number of insulin receptors on target cells [81] causes a reduction in fetal glucose uptake [82]. As a result, fetal protein mass is decreased and protein synthesis is lower than in controls [83].…”

Section: Gestational Diabetesmentioning

confidence: 99%

Experimental IUGR and later diabetes

Martin-Gronert

Ozanne

2007

Journal of Internal Medicine

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Abstract. Martin-Gronert MS, Ozanne SE (University of Cambridge, Cambridge, UK). Experimental IUGR and later diabetes (Symposium). J Intern Med 2007; 261: 437-452.It is widely accepted that an association exists between the intrauterine environment in which a fetus grows and develops and the subsequent development of type 2 diabetes. Any disturbance in maternal ability to provide nutrients and oxygen to the fetus can lead to fetal intrauterine growth restriction (IUGR). Here we will review IUGR in rodent models, in which maternal metabolism has been experimentally manipulated to investigate the molecular basis of the relationship between IUGR and development of type 2 diabetes in later life, and the identification of the molecular derangements in specific metabolicallysensitive organs/tissues.

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Maternal diabetes in rats. II. Effects on fetal growth and protein turnover

Cited by 21 publications

References 0 publications

Alterations in perivascular innervation function in mesenteric arteries from offspring of diabetic rats

Alterations in perivascular innervation function in mesenteric arteries from offspring of diabetic rats

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

Experimental IUGR and later diabetes

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