A brief study of mechanism, animal models, and management for obesity

Obesity appears as fat accumulation in adipose tissue from high energy intake and insufficient energy consumption. It is accompanied by several factors such as genetics, environmental, fetal nutrition, energy intake and expenditure, and culture. These factors stimulate several other mechanisms that contribute to obesity and obesity-related disorders such as hypertension, diabetes, arthritis, hyperlipidemia, coronary heart disease, etc. In the present article, we have examined the main factors, symptoms, and special problems associated with obesity, mechanisms of obesity, and the relation of important parameters with obesity. We have also depicted the various animal models for obesity research. Lastly, we have described the management of obesity.

FETAL ORIGIN OF ADULT DISEASE

“Fetal origins of adult disease”, often called the “Barker hypothesis” after a large proportion data of Barker and colleagues in Southampton over the last decade, that adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in structure, physiology, metabolism, which result in increased disease risk in adulthood. Many further studies have provided evidence for the hypothesis that size at birth is related to the risk of developing disease in later life. In particular, links are well established between reduced birthweight and increased risk of coronary heart disease, diabetes, hypertension and stroke in adulthood. The most widely accepted mechanisms thought to underlie these relationship are those of altered fetal nutrition, genetic–epigenetic links, fetal programming and fetal excess glucocorticoid exposure. It is suggested that the fetus makes physiological adaption in response to changes in its environment to prepare itself for posnatal life. The “Fetal origin of adult disease” hypothesis is attractive. It suggests that these diseases could be prevented by improving maternal health and fetal development

Placental Immune Responses to Viruses: Molecular and Histo-Pathologic Perspectives

As most recently demonstrated by the SARS-CoV-2 pandemic, congenital and perinatal infections are of significant concern to the pregnant population as compared to the general population. These outcomes can range from no apparent impact all the way to spontaneous abortion or fetal infection with long term developmental consequences. While some pathogens have developed mechanisms to cross the placenta and directly infect the fetus, other pathogens lead to an upregulation in maternal or placental inflammation that can indirectly cause harm. The placenta is a temporary, yet critical organ that serves multiple important functions during gestation including facilitation of fetal nutrition, oxygenation, and prevention of fetal infection in utero. Here, we review trophoblast cell immunology and the molecular mechanisms utilized to protect the fetus from infection. Lastly, we discuss consequences in the placenta when these protections fail and the histopathologic result following infection.

The Maternal Nutritional Buffering Model: an evolutionary framework for pregnancy nutritional intervention

Evidence that fetal nutrition influences adult health has heightened interest in nutritional interventions targeting pregnancy. However, as is true for other placental mammals, human females have evolved mechanisms that help buffer the fetus against short-term fluctuations in maternal diet and energy status. In this review, we first discuss the evolution of increasingly elaborate vertebrate strategies of buffering offspring from environmental fluctuations during development, including the important innovation of the eutherian placenta. We then present the Maternal Nutritional Buffering Model, which argues that, in contrast to many micronutrients that must be derived from dietary sources, the effects of short-term changes in maternal macronutrient intake during pregnancy, whether due to a deficit or supplementation, will be minimized by internal buffering mechanisms that work to ensure a stable supply of essential resources. In contrast to the minimal effects of brief macronutrient supplementation, there is growing evidence that sustained improvements in early life and adult pre-pregnancy nutrition could improve birth outcomes in offspring. Building on these and other observations, we propose that strategies to improve fetal macronutrient delivery will be most effective if they modify the pregnancy metabolism of mothers by targeting nutrition prior to conception and even during early development, as a complement to the conventional focus on bolstering macronutrient intake during pregnancy itself. Our model leads to the prediction that birth weight will be more strongly influenced by the mother’s chronic pre-pregnancy nutrition than by pregnancy diet, and highlights the need for policy solutions aimed at optimizing future, intergenerational health outcomes. Lay summary: We propose that strategies to improve fetal macronutrient delivery will be most effective if they modify the pregnancy metabolism of mothers by targeting nutrition prior to conception and even during early development, as a complement to the conventional focus on bolstering macronutrient intake during pregnancy itself.

The Role of microRNAs Identified in the Amniotic Fluid

Aim:The study aimed to provide an overall view of current data considering the presence of microRNAs in amniotic fluid.Methods:The available literature in MEDLINE, regarding the role of the amniotic fluid in pregnancy and fetal development, was searched for related articles including terms such as “microRNA”, “Amniotic fluid”, “Adverse outcome” and others.Results:The amniotic fluid has an undoubtedly significant part in fetal nutrition, with a protecting and thermoregulatory role alongside. MicroRNAs have proven to be highly expressed during pregnancy in many body liquids including amniotic fluid and are transferred between cells loaded in exosomes, while they are also implicated in many processes during fetal development and could be potential biomarkers for early prediction of adverse outcomes.Conclusion:Current knowledge reveals that amniotic fluid microRNAs participate in many developmental and physiological processes of pregnancy including proliferation of fibroblasts, fetal development, angiogenesis, cardioprotection, activation of signaling pathways, differentiation and cell motility, while the expression profile of specific microRNAs has a potential prognostic role in the prediction of Down syndrome, congenital hydronephrosis and kidney fibrosis.

Evolution of placentotrophy: using viviparous sharks as a model to understand vertebrate placental evolution

Reproducing sharks must provide their offspring with an adequate supply of nutrients to complete embryonic development. In oviparous (egg-laying) sharks, offspring develop outside the mother, and all the nutrients required for embryonic growth are contained in the egg yolk. Conversely, in viviparous (live-bearing) sharks, embryonic development is completed inside the mother, providing offspring with the opportunity to receive supplementary embryonic nourishment, known as matrotrophy. Viviparous sharks exhibit nearly all forms of matrotrophy known in vertebrates, including a yolk-sac placenta, which involves several significant ontogenetic modifications to fetal and maternal tissues. The selective pressures that have driven the evolution of complex placentas in some shark species, but not in others, are unresolved. Herein we review the mechanisms of reproductive allocation and placental diversity in sharks, and consider the application of both adaptive and conflict hypotheses for the evolution of placental nutrient provisioning. Both have likely played roles in placental evolution in sharks, perhaps at different times in evolutionary history. Finally, we recommend sharks as an outstanding model system to investigate the evolution of placentas and mechanisms for fetal nutrition during pregnancy in vertebrates.

Nutrition, the visceral immune system, and the evolutionary origins of pathogenic obesity

The global obesity epidemic is the subject of an immense, diversely specialized research effort. An evolutionary analysis reveals connections among disparate findings, starting with two well-documented facts: Obesity-associated illnesses (e.g., type-2 diabetes and cardiovascular disease), are especially common in: (i) adults with abdominal obesity, especially enlargement of visceral adipose tissue (VAT), a tissue with important immune functions; and (ii) individuals with poor fetal nutrition whose nutritional input increases later in life. I hypothesize that selection favored the evolution of increased lifelong investment in VAT in individuals likely to suffer lifelong malnutrition because of its importance in fighting intraabdominal infections. Then, when increased nutrition violates the adaptive fetal prediction of lifelong nutritional deficit, preferential VAT investment could contribute to abdominal obesity and chronic inflammatory disease. VAT prioritization may help explain several patterns of nutrition-related disease: the paradoxical increase of chronic disease with increased food availability in recently urbanized and migrant populations; correlations between poor fetal nutrition, improved childhood (catch-up) growth, and adult metabolic syndrome; and survival differences between children with marasmus and kwashiorkor malnutrition. Fats and sugars can aggravate chronic inflammation via effects on intestinal bacteria regulating gut permeability to visceral pathogens. The extremes in a nutrition-sensitive trade-off between visceral (immune-function) vs. subcutaneous (body shape) adiposity may have been favored by selection in highly stratified premedicine societies. Altered adipose allocation in populations with long histories of social stratification and malnutrition may be the result of genetic accommodation of developmental responses to poor maternal/fetal conditions, increasing their vulnerability to inflammatory disease.