Maternal underweight and obesity are associated with placental pathologies in human pregnancy

Introduction: Maternal underweight and obesity are prevalent conditions, associated with chronic, low-grade inflammation, poor fetal development, and long-term adverse outcomes for the child. The placenta senses and adapts to the pregnancy environment in an effort to support optimal fetal development. However, the mechanisms driving these adaptations, and the resulting placental phenotypes, are poorly understood. We hypothesised that maternal underweight and obesity would be associated with increased prevalence of placental pathologies in term and preterm pregnancies. Methods: Data from 12,154 pregnancies were obtained from the Collaborative Perinatal Project, a prospective cohort study conducted from 1959 to 1974. Macro and microscopic placental pathologies were analysed across maternal prepregnancy body mass index (BMI) to assess differences in the presence of pathologies among underweight, overweight, and obese BMI groups compared to normal weight reference BMI at term and preterm. Placental pathologies were also assessed across fetal sex. Results: Pregnancies complicated by obesity had placentae with increased fetal inflammation at preterm and increased maternal inflammation at term. In term pregnancies, increasing maternal BMI associated with increased maternal vascular malperfusion (MVM), odds of an appropriate mature placenta for gestational age, and placental weight, and decreased placental efficiency. Male placentae, independent of maternal BMI, had increased inflammation, MVM, and placental efficiency than female placentae, particularly at term. Discussion: Maternal underweight and obesity are not inert conditions for the placenta, and the histomorphological changes driven by suboptimal maternal BMI may serve as indicators of adversities experienced in utero and potential predictors of future health trajectories.

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PCOS without hyperandrogenism is associated with higher plasma Trimethylamine N-oxide levels

BMC Endocrine Disorders ◽

10.1186/s12902-019-0486-9 ◽

2020 ◽

Vol 20 (1) ◽

Cited By ~ 2

Author(s):

Jiayu Huang ◽

Lin Liu ◽

Chunyan Chen ◽

Ying Gao

Keyword(s):

Insulin Resistance ◽

Polycystic Ovary ◽

Predictive Biomarker ◽

Normal Weight ◽

Inflammatory Factors ◽

Low Grade ◽

Model Assessment ◽

Increased Risk ◽

Homeostatic Model Assessment ◽

Low Grade Inflammation

Abstract Background Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder, and its pathogenesis is still under debate. Trimethylamine-N-oxide (TMAO) is a small, organic compound generated by the gut microbiome with a hypothesized relation to insulin resistance (IR) and low-grade inflammation in PCOS. By comparing plasma TMAO levels in non-PCOS participants and PCOS patients without hyperandrogenism (HA), we aimed to determine whether plasma TMAO levels correlate with PCOS without HA and to analyze their relationship with low-grade inflammation and IR. Methods A total of 27 PCOS patients without HA and 23 non-PCOS participants were enrolled in this study and subdivided into “nonobese” and “obese” arms for each group. Levels of plasma TMAO were quantified, and basic clinical characteristics and plasma biomarkers of inflammation were assessed. Results First, plasma TMAO levels, insulin levels and homeostatic model assessment of insulin resistance (HOMA-IR) values were higher in PCOS patients without HA, especially in the obese subgroup. Second, the levels of the inflammatory factors interleukin (IL)-17A, IL-18 and interferon gamma (IFN-γ) were significantly increased in obese PCOS patients without HA. Third, plasma TMAO levels were associated with body mass index (BMI) in the normal-weight groups, and the obese groups had higher fasting plasma insulin (FINS) and HOMA-IR values. Finally, logistic regression showed that the plasma levels of TMAO and luteinizing hormone/follicle-stimulating hormone (LH/FSH) were independent predictors of PCOS and indicated an increased risk of PCOS. Conclusions Elevated plasma TMAO levels may be associated with the pathogenesis of PCOS without HA and correlated with increased systemic inflammation. Further studies are needed to determine the suitability of TMAO as a predictive biomarker and to identify possible therapies for PCOS.

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Serum IL-12 Is Increased in Mexican Obese Subjects and Associated with Low-Grade Inflammation and Obesity-Related Parameters

Mediators of Inflammation ◽

10.1155/2013/967067 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 28

Author(s):

K. Suárez-Álvarez ◽

L. Solís-Lozano ◽

S. Leon-Cabrera ◽

A. González-Chávez ◽

G. Gómez-Hernández ◽

...

Keyword(s):

Body Fat ◽

Adult Population ◽

Strong Relationship ◽

Normal Weight ◽

Low Grade ◽

Body Fat Percentage ◽

Fat Percentage ◽

Necrosis Factor Alpha ◽

Obese Subjects ◽

Low Grade Inflammation

Interleukin-(IL-) 12 has been recently suggested to participate during development of insulin resistance in obese mice. Nevertheless, serum IL-12 levels have not been accurately determined in overweight and obese humans. We thus studied serum concentrations of IL-12 in Mexican adult individuals, examining their relationship with low-grade inflammation and obesity-related parameters. A total of 147 healthy individuals, 43 normal weight, 61 overweight, and 43 obese subjects participated in the study. Circulating levels of IL-12, tumor necrosis factor-alpha (TNF-α), leptin, insulin, glucose, total cholesterol, and triglyceride were measured after overnight fasting in all of the study subjects. Waist circumference and body fat percentage were recorded for all the participants. Serum IL-12 was significantly higher in overweight and obese individuals than in normal weight controls. Besides being strongly related with body mass index (r=0.5154), serum IL-12 exhibited a significant relationship with abdominal obesity (r=0.4481), body fat percentage (r=0.5625), serum glucose (r=0.3158), triglyceride (r=0.3714), and TNF-α(r=0.4717). Thus, serum levels of IL-12 are increased in overweight and obese individuals and show a strong relationship with markers of low-grade inflammation and obesity in the Mexican adult population. Further research is needed to understand the role of IL-12 in developing obesity-associated alterations in humans.

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Substantial fat mass loss reduces low-grade inflammation and induces positive alteration in cardiometabolic factors in normal-weight individuals

Scientific Reports ◽

10.1038/s41598-019-40107-6 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 5

Author(s):

H. V. Sarin ◽

J. H. Lee ◽

M. Jauhiainen ◽

A. Joensuu ◽

K. Borodulin ◽

...

Keyword(s):

Mass Loss ◽

Fat Mass ◽

Normal Weight ◽

Low Grade ◽

Low Grade Inflammation ◽

Fat Mass Loss ◽

Cardiometabolic Factors

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Oxidative Stress and Low-Grade Inflammation in Polycystic Ovary Syndrome: Controversies and New Insights

International Journal of Molecular Sciences ◽

10.3390/ijms22041667 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1667 ◽

Cited By ~ 1

Author(s):

Antonio Mancini ◽

Carmine Bruno ◽

Edoardo Vergani ◽

Claudia d’Abate ◽

Elena Giacchi ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Vitamin D ◽

Polycystic Ovary Syndrome ◽

Polycystic Ovary ◽

Normal Weight ◽

Low Grade ◽

Ovary Syndrome ◽

Low Grade Inflammation

The pathophysiology of Polycystic Ovary Syndrome (PCOS) is quite complex and different mechanisms could contribute to hyperandrogenism and anovulation, which are the main features of the syndrome. Obesity and insulin-resistance are claimed as the principal factors contributing to the clinical presentation; in normal weight PCOS either, increased visceral adipose tissue has been described. However, their role is still debated, as debated are the biochemical markers linked to obesity per se. Oxidative stress (OS) and low-grade inflammation (LGI) have recently been a matter of researcher attention; they can influence each other in a reciprocal vicious cycle. In this review, we summarize the main mechanism of radical generation and the link with LGI. Furthermore, we discuss papers in favor or against the role of obesity as the first pathogenetic factor, and show how OS itself, on the contrary, can induce obesity and insulin resistance; in particular, the role of GH-IGF-1 axis is highlighted. Finally, the possible consequences on vitamin D synthesis and activation on the immune system are briefly discussed. This review intends to underline the key role of oxidative stress and low-grade inflammation in the physiopathology of PCOS, they can cause or worsen obesity, insulin-resistance, vitamin D deficiency, and immune dyscrasia, suggesting an inverse interaction to what is usually considered.

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Inflammatory Bowel Diseases and Sarcopenia: The Role of Inflammation and Gut Microbiota in the Development of Muscle Failure

Frontiers in Immunology ◽

10.3389/fimmu.2021.694217 ◽

2021 ◽

Vol 12 ◽

Author(s):

Olga Maria Nardone ◽

Roberto de Sire ◽

Valentina Petito ◽

Anna Testa ◽

Guido Villani ◽

...

Keyword(s):

Gut Microbiota ◽

Adverse Outcomes ◽

Low Grade ◽

Increased Risk ◽

Bowel Diseases ◽

Inflammatory Bowel ◽

And Function ◽

Host Metabolism ◽

Low Grade Inflammation

Sarcopenia represents a major health burden in industrialized country by reducing substantially the quality of life. Indeed, it is characterized by a progressive and generalized loss of muscle mass and function, leading to an increased risk of adverse outcomes and hospitalizations. Several factors are involved in the pathogenesis of sarcopenia, such as aging, inflammation, mitochondrial dysfunction, and insulin resistance. Recently, it has been reported that more than one third of inflammatory bowel disease (IBD) patients suffered from sarcopenia. Notably, the role of gut microbiota (GM) in developing muscle failure in IBD patient is a matter of increasing interest. It has been hypothesized that gut dysbiosis, that typically characterizes IBD, might alter the immune response and host metabolism, promoting a low-grade inflammation status able to up-regulate several molecular pathways related to sarcopenia. Therefore, we aim to describe the basis of IBD-related sarcopenia and provide the rationale for new potential therapeutic targets that may regulate the gut-muscle axis in IBD patients.

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TLR4-NF-κB Signal Involved in Depressive-Like Behaviors and Cytokine Expression of Frontal Cortex and Hippocampus in Stressed C57BL/6 and ob/ob Mice

Neural Plasticity ◽

10.1155/2018/7254016 ◽

2018 ◽

Vol 2018 ◽

pp. 1-12 ◽

Cited By ~ 20

Author(s):

Yihe Wang ◽

Jingjing Xu ◽

Yuan Liu ◽

Ziyang Li ◽

Xiaohong Li

Keyword(s):

Frontal Cortex ◽

Normal Weight ◽

Behavioral Disorder ◽

Low Grade ◽

Mild Stress ◽

Obese Mice ◽

Serum Corticosterone ◽

Low Grade Inflammation ◽

Necrosis Factor

Studies found that elevated levels of cytokines such as interleukin- (IL-) 1β, IL-6, and tumor necrosis factor-α (TNF-α) are closely associated with the pathogenesis of depression. Obesity providing a low-grade inflammation state was proposed to be implicated in susceptibility to depression in obesity. However, the alterations of cytokines and the TLR4-NF-κB signal in the brain of normal-weight and obese mice under stress have not been fully elucidated. This study used chronic unpredictable mild stress (CUMS) to induce a depressive-like behavior in an animal model and examine depressive-like behaviors, memory changes, and serum corticosterone levels, as well as the expressions of cytokines and NF-κB in the frontal cortex and hippocampus. We aimed to observe the role of neuroinflammation in susceptibility to depression in obesity under CUMS. In addition, we investigated the protective effect of inhibiting the TLR4-NF-κB signal. Our results demonstrated that CUMS induced depressive-like behavior and spatial memory damage, higher level of serum corticosterone, and overexpression of cytokines and NF-κB in the frontal cortex and hippocampus in both C57BL/6 and ob/ob mice. ob/ob mice displayed serious behavioral disorder and higher levels of IL-1β, IL-6, TNF-α, and NF-κB. Our results concluded that a hyperactive TLR4-NF-κB signal and higher level of cytokines are involved in susceptibility to depression in stressed obese mice.

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COVID-19 and Obesity: Overlapping of Two Pandemics

Obesity Facts ◽

10.1159/000518386 ◽

2021 ◽

pp. 1-7

Author(s):

Maria Alessandra Gammone ◽

Nicolantonio D’Orazio

Keyword(s):

Adipose Tissue ◽

Critical Illness ◽

Strong Correlation ◽

Metabolic Disorders ◽

Therapeutic Potential ◽

Adverse Outcomes ◽

Severe Illness ◽

Low Grade ◽

Obese Patients ◽

Low Grade Inflammation

Background: The coronavirus disease 2019 (COVID-19) pandemic has recently led to worldwide research efforts to identify subjects at greater risk of developing more severe illness: overall obesity displayed a strong correlation with critical illness and major severity of COVID-19 manifestations. Summary: Obesity and metabolic disorders are closely linked to chronic systemic inflammation. The adipose tissue constitutes a source of cytokines, which configure a low-grade inflammation and a hypercoagulation status; in addition, diagnosis and care of obese patients are often complicated by excess weight and ventilation difficulties. Key Messages: This review aims to examine the intersection between obesity and adverse outcomes of COVID-19, in order to investigate its preventive and/or therapeutic potential in the management of obesity-related COVID-19 complications.

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Effects of different levels of physical inactivity on plasma visfatin in healthy normal-weight men

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2012-0434 ◽

2013 ◽

Vol 38 (6) ◽

pp. 689-693 ◽

Cited By ~ 5

Author(s):

Floriane Rudwill ◽

Stéphane Blanc ◽

Guillemette Gauquelin-Koch ◽

Alexander Choukèr ◽

Martina Heer ◽

...

Keyword(s):

Physical Inactivity ◽

Independent Predictor ◽

Bed Rest ◽

Normal Weight ◽

Low Grade ◽

Healthy Men ◽

Low Grade Inflammation ◽

The Relationship ◽

Different Levels ◽

Activity Energy

We tested whether physical inactivity (PI) is an independent predictor of plasma visfatin, a newly discovered adipokine likely involved in the relationship between obesity-associated low-grade inflammation and insulin resistance. PI was induced in healthy men (Body Mass Index = 23.4 ± 0.6 kg·m−2) by 10 days of confinement (n = 8), 1 month of detraining (n = 10), and 3 months of bed rest with (n = 7) and without exercise (n = 8). Visfatin was negatively associated with activity energy expenditure (p = 0.03). No relationship was observed with insulin sensitivity. This suggested that PI itself increases visfatin concentrations.

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