scholarly journals An examination of maternal contributors and potential modifiers of fetal growth in pregnancy

2013 ◽  
Vol 38 (3) ◽  
pp. 360-360 ◽  
Author(s):  
Zachary M. Ferraro
Keyword(s):  
Physical Activity ◽  
Body Weight ◽  
Weight Gain ◽  
Pregnant Women ◽  
Maternal Obesity ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Fetal Outcomes ◽  
Igfbp 3

A greater understanding of critical periods of body weight regulation, including pregnancy, may aid in efforts to optimize weight management strategies for the mother and her baby. The gestational period has been implicated to play, in the child, a vital role in the developmental origins of obesity and other cardiometabolic diseases later in life. Therefore, we initially examined existing literature on the role of maternal obesity and its link to pediatric obesity and documented the known underlying physiological mechanisms responsible for this relationship, while suggesting potential intervention targets that may improve maternal–fetal outcomes. In a second paper, we aimed to quantify maternal predictors of large for gestational-age neonates in the Ottawa and Kingston birth cohort with specific hypotheses verifying the independent contribution of maternal prepregnancy body mass index (BMI) and excessive gestational weight gain (GWG) to fetal overgrowth. This paper also highlighted the clinical utility of the revised 2009 Institute of Medicine GWG guidelines and discussed the potential role of physiological factors underlying the observed associations. As follow-ups to our population-level analysis, papers 3 and 4 highlighted how the insulin-like growth factor (IGF) axis, a vital regulator of growth and development, may be compromised at the molecular level in cases of maternal obesity (paper 3) and excessive GWG (paper 4). In paper 3, we showed that maternal obesity is associated with attenuated expression of IGF binding protein-4 (IGFBP-4) in umbilical cord blood and discussed how this may preferentially promote fetal adipogenesis. The effects of excessive GWG on IGF axis protein expression were addressed in paper 4, where we showed that independent of prepregnancy BMI, excessive weight gain during pregnancy is associated with increased expression of IGFBP-3 in maternal circulation in normoglycemic term pregnancies. In that paper we discussed the potential inhibitory role of IGFBP-3 on adipogenesis and how it relates to glucose intolerance during pregnancy. Recognizing that both obesity and excessive GWG can alter physiological processes in a mother and her baby, we concluded that appropriate evidence-based interventions are warranted to best optimize outcomes. In paper 5, we discussed the results of a study that sought to assess patient information channels and knowledge of nutrition and physical activity during pregnancy. The intent was that these findings be applied to best-design efficacious strategies that cater to the needs of our target group of pregnant women. In our analysis we showed that the majority of pregnant women studied would be willing to participate in a lifestyle intervention for their own personal health and that of their child. Of great interest was the observation that most women were not informed of the importance of pregnancy-specific energy intake, or made aware of their own healthy GWG targets. Additionally, many of the respondents reported that they did not receive information that pertained to appropriate physical activity recommendations, even though the vast majority of participants considered this lifestyle modality to be safe during their pregnancy. Finally, in paper 6 we built on the results of our previous work and evaluated the risks and benefits of physical activity during pregnancy on maternal–fetal outcomes through a review of the literature and noted that engaging in nonsedentary pursuits during gestation may aid in maternal weight regulation, protect against metabolic disorders, and optimize neonatal birth weight and body composition. Overall, the collective nature of the papers presented in this dissertation provides qualitative and quantitative evidence to support not only the complexity of body weight regulation in the mother and her baby, but also highlights potential avenues for intervention that may improve maternal–fetal outcomes during this critical period.

scholarly journals Role of Physical Activity and Exercise in Treating Patients with Overweight and Obesity

2018 ◽  
Vol 64 (1) ◽  
pp. 99-107 ◽  
Author(s):  
John M Jakicic ◽  
Renee J Rogers ◽  
Kelliann K Davis ◽  
Katherine A Collins
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Overweight And Obesity ◽  
Current Evidence ◽  
Dietary Modification ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Lifestyle Behavior

Abstract BACKGROUND Overweight and obesity are significant public health concerns that are linked to numerous negative health consequences. Physical activity is an important lifestyle behavior that contributes to body weight regulation. CONTENT Physical activity is inversely associated with weight gain and the incidence of obesity. Physical activity also contributes to additional weight loss when coupled with dietary modification, and it can result in modest weight loss when not coupled with dietary modification. Moreover, physical activity is associated with improved long-term weight loss and prevention of weight gain following initial weight loss. Current evidence supports that physical activity should be moderate to vigorous in intensity to influence body weight regulation. There is also a growing body of evidence that physical activity can be accumulated throughout the day in shorter periods of time rather than being performed during a structured and longer period, and that physical activity performed in this manner can be important for body weight regulation. SUMMARY The literature supports the inclusion of physical activity as an important lifestyle behavior for regulating body weight. There are multiple intervention approaches that may be effective for enhancing physical activity engagement within the context of weight control.

scholarly journals Dietary Isoflavone-Dependent and Estradiol Replacement Effects on Body Weight in the Ovariectomized (OVX) Rat

2017 ◽  
Vol 49 (06) ◽  
pp. 457-465 ◽  
Author(s):  
Ashley Russell ◽  
Jamie Grimes ◽  
Danette Cruthirds ◽  
Joanna Westerfield ◽  
Lawren Wooten ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Metabolism ◽  
Body Weight Gain ◽  
Abdominal Fat ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Estradiol Treatment ◽  
Serum Leptin ◽  
Cytokines And Chemokines

Abstract17β-Estradiol is known to regulate energy metabolism and body weight. Ovariectomy results in body weight gain while estradiol administration results in a reversal of weight gain. Isoflavones, found in rodent chow, can mimic estrogenic effects making it crucial to understand the role of these compounds on metabolic regulation. The goal of this study is to examine the effect of dietary isoflavones on body weight regulation in the ovariectomized rat. This study will examine how dietary isoflavones can interact with estradiol treatment to affect body weight. Consistent with previous findings, animals fed an isoflavone-rich diet had decreased body weight (p<0.05), abdominal fat (p<0.05), and serum leptin levels (p<0.05) compared to animals fed an isoflavone-free diet. Estradiol replacement resulted in decreased body weight (p<0.05), abdominal fat (p<0.05), and serum leptin (p<0.05). Current literature suggests the involvement of cytokines in the inflammatory response of body weight gain. We screened a host of cytokines and chemokines that may be altered by dietary isoflavones or estradiol replacement. Serum cytokine analysis revealed significant (p<0.05) diet-dependent increases in inflammatory cytokines (keratinocyte-derived chemokine). The isoflavone-free diet in OVX rats resulted in the regulation of the following cytokines and chemokines: interleukin-10, interleukin-18, serum regulated on activation, normal T cell expressed and secreted, and monocyte chemoattractant protein-1 (p<0.05). Overall, these results reveal that estradiol treatment can have differential effects on energy metabolism and body weight regulation depending on the presence of isoflavones in rodent chow.

Pharmacological treatment strategies for patients with monogenic obesity

2020 ◽  
Vol 33 (8) ◽  
pp. 967-973
Author(s):  
Peter Kühnen ◽  
Susanna Wiegand ◽  
Heike Biebermann
Keyword(s):  
Body Weight ◽  
Pharmacological Treatment ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Research Progress ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Melanocortin Signaling ◽  
Recent Research Progress

AbstractThe leptin melanocortin signaling pathway is playing a pivotal role for body weight regulation. Genetic defects within this cascade are leading to severe hyperphagia and early onset obesity. In most cases, due to persistent hyperphagia the affected patients are not able to stabilize body weight for a longer period of time with conservative treatment strategies based on lifestyle interventions. Therefore, it is of importance to implement alternative treatment options for these patients. This review provides an overview about the published pharmacological treatment attempts in respect to monogenic forms of obesity and summarizes recent research progress about the role of MC4R signaling and POMC derivatives for body weight regulation.

scholarly journals Role of GABA Release From Leptin Receptor-Expressing Neurons in Body Weight Regulation

Endocrinology ◽  
2012 ◽  
Vol 153 (5) ◽  
pp. 2223-2233 ◽  
Author(s):  
Yuanzhong Xu ◽  
William G. O'Brien ◽  
Cheng-Chi Lee ◽  
Martin G. Myers ◽  
Qingchun Tong
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Leptin Receptor ◽  
Gaba Release ◽  
Neuron Activity ◽  
Chow Diet ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
The Brain

It is well established that leptin regulates energy balance largely through isoform B leptin receptor-expressing neurons (LepR neurons) in the brain and that leptin activates one subset of LepR neurons (leptin-excited neurons) while inhibiting the other (leptin-inhibited neurons). However, the neurotransmitters released from LepR neurons that mediate leptin action in the brain are not well understood. Previous results demonstrate that leptin mainly acts on γ-aminobutyric acid (GABA)ergic neurons to reduce body weight, and that leptin activates proopiomelanocortin neuron activity by reducing GABA release onto these neurons, suggesting a body weight-promoting role for GABA released from leptin-inhibited neurons. To directly examine the role of GABA release from LepR neurons in body weight regulation, mice with disruption of GABA release specifically from LepR neurons were generated by deletion of vesicular GABA transporter in LepR neurons. Interestingly, these mice developed mild obesity on chow diet and were sensitive to diet-induced obesity, which were associated with higher food intake and lower energy expenditure. Moreover, these mice showed blunted responses in both food intake and body weight to acute leptin administration. These results demonstrate that GABA plays an important role in mediating leptin action. In combination with the previous studies that leptin reduces GABA release onto proopiomelanocortin neurons through leptin-inhibited neurons and that disruption of GABA release from agouti gene-related protein neurons, one subset of LepR-inhibited neurons, leads to a lean phenotype, our results suggest that, under our experimental conditions, GABA release from leptin-excited neuron dominates over leptin-inhibited ones.

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