Role of adipose tissue in regulating fetal growth in gestational diabetes mellitus.

Placenta

Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia; Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia. Electronic address:

Published: December 2020

AI Article Synopsis

  • Gestational diabetes mellitus (GDM) poses serious health risks for both mothers and babies, highlighting the urgent need for effective treatments.
  • The interplay between adipose tissue, the placenta, and fetal growth is crucial, as the placenta controls how nutrients are transferred to the fetus.
  • This review focuses on how factors from adipose tissue influence placental nutrient transporters, suggesting that understanding these interactions could lead to new ways to prevent GDM.

Article Abstract

Gestational diabetes mellitus (GDM) is a global health issue with significant short and long-term complications for both mother and baby. There is a strong need to identify an effective therapeutic that can prevent the development of GDM. A better understanding of the pathophysiology of GDM and the relationship between the adipose tissue, the placenta and fetal growth is required. The placenta regulates fetal growth by modulating nutrient transfer of glucose, amino acids and fatty acids. Various factors secreted by the adipose tissue, such as adipokines, adipocytokines and more recently identified extracellular vesicles, can influence inflammation and interact with placental nutrient transport. In this review, the role of the placental nutrient transporters and the adipose-derived factors that can influence their function will be discussed. A better understanding of these factors and their relationship may make a potential target for therapeutic interventions to prevent the development of GDM and its consequences.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.placenta.2020.05.006DOI Listing

Publication Analysis

Top Keywords

adipose tissue
12
fetal growth
12
gestational diabetes
8
diabetes mellitus
8
prevent development
8
development gdm
8
better understanding
8
placental nutrient
8
role adipose
4
tissue regulating
4

Similar Publications

PURPOSE OF REVIEW: Narrative review of the author's main contributions to the field of cardiovascular health spanning four decades, with a focus on findings related to 1- the pathophysiology of obesity, insulin resistance, type 2 diabetes and cardiovascular disease, and 2- the management/prevention of these conditions. Particular attention is given to the importance of regular physical activity. RECENT FINDINGS: Because behaviors and their physiological consequences are still not measured in clinical practice, it is proposed to systematically assess and target "lifestyle vital signs" (waist circumference, cardiorespiratory fitness, food-based diet quality and level of leisure-time physical activity) in primary care.

View Article and Find Full Text PDF

Bone Marrow Adipocytes as Novel Regulators of Metabolic Homeostasis: Clinical Consequences of Bone Marrow Adiposity.

Curr Obes Rep

January 2025

Maine Medical Center Research Institute, Maine Medical Center, 81 Research Drive, Scarborough, ME, 04074, USA.

Purpose Of Review: Bone marrow adipose tissue is a distinctive fat depot located within the skeleton, with the potential to influence both local and systemic metabolic processes. Although significant strides have been made in understanding bone marrow adipose tissue over the past decade, many questions remain regarding their precise lineage and functional roles.

Recent Findings: Recent studies have highlighted bone marrow adipose tissue's involvement in continuous cross-talk with other organs and systems, exerting both endocrine and paracrine functions that play a crucial role in metabolic homeostasis, skeletal remodeling, hematopoiesis, and the progression of bone metastases.

View Article and Find Full Text PDF

Background: We aimed to evaluate how the parameters used in the diagnosis of metabolic syndrome (MetS) and parameters such as epicardial adipose tissue (EAT) thickness, insulin resistance (IR), and serum uric acid (SUA) are affected according to the severity of obesity.

Methods: A total of 120 obese patients aged 10-18 years were classified as class 1-2-3 according to their body mass index (BMI) score. SUA was measured and oral glucose tolerance tests were performed on all patients.

View Article and Find Full Text PDF

Metabolic syndrome-related diseases frequently involve disturbances in skeletal muscle lipid metabolism. The accumulation of lipid metabolites, lipid-induced mitochondrial stress in skeletal muscle cells, as well as the inflammation of adjacent adipose tissue, are associated with the development of insulin resistance and metabolic dysfunction. Consequently, when antidiabetic medications are used to treat various chronic conditions related to hyperglycaemia, the impact on skeletal muscle lipid metabolism should not be overlooked.

View Article and Find Full Text PDF

The hypothalamus integrates peripheral signals and modulates food intake and energy expenditure by regulating the metabolic function of peripheral tissues, including the liver and adipose tissue. In a previous study, we demonstrated that s-resistin, an intracellular resistin isoform highly expressed in the hypothalamus and upregulated during aging, is important in the central control of energy homeostasis, affecting mainly the peripheral response to insulin by still unknown mechanisms. Herein, using an intracerebroventricular injection of a specific lentiviral RNAi against s-resistin, we assessed, in the Wistar rat, the effects of central s-resistin downregulation on the expression and phosphorylation levels of intermediates involved in insulin signaling and the inflammatory response in epididymal white adipose tissue (eWAT) and liver.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!