Framing the discussion of microorganisms as a facet of social equity in human health

What do “microbes” have to do with social equity? These microorganisms are integral to our health, that of our natural environment, and even the “health” of the environments we build. The loss, gain, and retention of microorganisms—their flow between humans and the environment—can greatly impact our health. It is well-known that inequalities in access to perinatal care, healthy foods, quality housing, and the natural environment can create and arise from social inequality. Here, we focus on the argument that access to beneficial microorganisms is a facet of public health, and health inequality may be compounded by inequitable microbial exposure

Intergenerational effects of maternal obesity on offspring mitochondrial reactive oxygen species production and DNA damage

Project files are comprised of 1 page pdf and presentation recording in mp4 format.Epidemiological studies have shown that offspring from pregnancies complicated by maternal obesity have a 4-fold greater risk for developing childhood obesity and symptoms of metabolic syndrome. The developmental origins of health and disease (DOHaD) hypothesis states that certain environmental exposures during critical windows of development may have consequences for an individuals long term health. DOHaD may explain a portion of the continual increase in obesity rates among children. In a non-human primate model, offspring of  obese dams become sensitized to obesity-induced metabolic disruptions, including insulin resistance and mitochondrial disfunction. Increased reactive oxygen species (ROS) production contributes to mitochondrial defects observed in obesity. Oxidative stress, which is caused by overproduction of ROS, can lead to mitochondrial DNA (mtDNA) mutations, decreased copy number, reduced membrane permeability and subsequent suppression of mitochondrial respiratory chain activity. Therefore, I hypothesize that maternal obesity increases offspring mitochondrial ROS production leading to mtDNA damage without loss of mtDNA abundance. To study the effect of maternal obesity, we used a previously established Japanese macaque model of fetal programming. Dams were fed either a control (CON) diet or western style diet (WSD) prior to and during pregnancy and lactation. Offspring were then weaned at 8 months and fed a healthy CON diet. Skeletal muscle biopsies from offspring were collected at 3 years of age and relative mtDNA abundance was measured using quantitative PCR (qPCR) amplification of short regions of mtDNA. No differences were measured in the amount of mtDNA between offspring groups. Moving forward, I will test for elevations in ROS-induced mtDNA damage by qPCR amplification. Overall, these data indicate that exposure to maternal obesity and WSD during fetal development does not reduce mitochondrial abundance in skeletal muscle of adolescent offspring. Further tests are needed to determine whether observed reductions in mitochondrial homeostasis are linked to elevated ROS production.NIH 1R24DK090964-01 to Carrie E. McCurdy, Undergraduate Research Opportunity Program Mini-Gran

Intergenerational Effects of Maternal Obesity on Offspring Mitochondrial Reactive Oxygen Species Production and DNA Damage

28 pages. A thesis presented to the Department of Human Physiology and the Clark Honors College of the University of Oregon in partial fulfillment of the requirements for degree of Bachelor of Science], Winter 2021.Epidemiological studies have shown that offspring from pregnancies complicated by maternal obesity have a 4-fold greater risk for developing childhood obesity and symptoms of metabolic syndrome. The developmental origins of health and disease (DOHaD) hypothesis states that certain environmental exposures during critical windows of development may have consequences for an individual’s long term health. DOHaD may explain a portion of the continual increase in obesity rates among children. In a nonhuman primate model, offspring of obese dams become sensitized to obesity-induced metabolic disruptions, including insulin resistance and mitochondrial disfunction. Increased reactive oxygen species (ROS) production contributes to mitochondrial defects observed in obesity. Oxidative stress, which is caused by overproduction of ROS, can lead to mitochondrial DNA (mtDNA) mutations, decreased copy number, reduced membrane permeability and subsequent suppression of mitochondrial respiratory chain activity. Therefore, I hypothesize that maternal obesity increases offspring mitochondrial ROS production leading to mtDNA damage without loss of mtDNA abundance. To study the effect of maternal obesity, we used a previously established Japanese macaque model of fetal programming. Dams were fed either a control (CON) diet or western style diet (WSD) prior to and during pregnancy and lactation. Offspring were then weaned at 8 months and fed a healthy CON diet. Skeletal muscle biopsies from offspring were collected at 3 years of age and relative mtDNA abundance was measured using quantitative PCR (qPCR) amplification of short regions of mtDNA. No differences were measured in the amount of mtDNA between offspring groups. Similarly, no differences were measured in the amount of mtDNA damage between offspring groups. Overall, these data indicate that exposure to maternal obesity and WSD during fetal development does not reduce mitochondrial abundance or alter mitochondrial homeostasis that is linked to ROS production in skeletal muscle of adolescent offspring

Intergenerational Effects of Maternal Obesity on Offspring Mitochondrial Reactive Oxygen Species Production and DNA Damage

Epidemiological studies have shown that offspring from pregnancies complicated by maternal obesity have a 4-fold greater risk for developing childhood obesity and symptoms of metabolic syndrome. The developmental origins of health and disease (DOHaD) hypothesis states that certain environmental exposures during critical windows of development may have consequences for an individual’s long term health. DOHaD may explain a portion of the continual increase in obesity rates among children. In a nonhuman primate model, offspring of obese dams become sensitized to obesity-induced metabolic disruptions, including insulin resistance and mitochondrial disfunction. Increased reactive oxygen species (ROS) production contributes to mitochondrial defects observed in obesity. Oxidative stress, which is caused by overproduction of ROS, can lead to mitochondrial DNA (mtDNA) mutations, decreased copy number, reduced membrane permeability and subsequent suppression of mitochondrial respiratory chain activity. Therefore, I hypothesize that maternal obesity increases offspring mitochondrial ROS production leading to mtDNA damage without loss of mtDNA abundance. To study the effect of maternal obesity, we used a previously established Japanese macaque model of fetal programming. Dams were fed either a control (CON) diet or western style diet (WSD) prior to and during pregnancy and lactation. Offspring were then weaned at 8 months and fed a healthy CON diet. Skeletal muscle biopsies from offspring were collected at 3 years of age and relative mtDNA abundance was measured using quantitative PCR (qPCR) amplification of short regions of mtDNA. No differences were measured in the amount of mtDNA between offspring groups. Similarly, no differences were measured in the amount of mtDNA damage between offspring groups. Overall, these data indicate that exposure to maternal obesity and WSD during fetal development does not reduce mitochondrial abundance or alter mitochondrial homeostasis that is linked to ROS production in skeletal muscle of adolescent offspring

Framing the discussion of microorganisms as a facet of social equity in human health.

What do "microbes" have to do with social equity? These microorganisms are integral to our health, that of our natural environment, and even the "health" of the environments we build. The loss, gain, and retention of microorganisms-their flow between humans and the environment-can greatly impact our health. It is well-known that inequalities in access to perinatal care, healthy foods, quality housing, and the natural environment can create and arise from social inequality. Here, we focus on the argument that access to beneficial microorganisms is a facet of public health, and health inequality may be compounded by inequitable microbial exposure