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1.
Allergy ; 77(5): 1389-1407, 2022 05.
Article in English | MEDLINE | ID: mdl-35073410

ABSTRACT

There is increasing understanding, globally, that climate change and increased pollution will have a profound and mostly harmful effect on human health. This review brings together international experts to describe both the direct (such as heat waves) and indirect (such as vector-borne disease incidence) health impacts of climate change. These impacts vary depending on vulnerability (i.e., existing diseases) and the international, economic, political, and environmental context. This unique review also expands on these issues to address a third category of potential longer-term impacts on global health: famine, population dislocation, and environmental justice and education. This scholarly resource explores these issues fully, linking them to global health in urban and rural settings in developed and developing countries. The review finishes with a practical discussion of action that health professionals around the world in our field can yet take.


Subject(s)
Climate Change , Global Health , Environmental Pollution , Humans
2.
PLoS Biol ; 17(12): e3000242, 2019 12.
Article in English | MEDLINE | ID: mdl-31805041

ABSTRACT

The ability to coordinate behavioral responses with metabolic status is fundamental to the maintenance of energy homeostasis. In numerous species including Caenorhabditis elegans and mammals, neural serotonin signaling regulates a range of food-related behaviors. However, the mechanisms that integrate metabolic information with serotonergic circuits are poorly characterized. Here, we identify metabolic, molecular, and cellular components of a circuit that links peripheral metabolic state to serotonin-regulated behaviors in C. elegans. We find that blocking the entry of fatty acyl coenzyme As (CoAs) into peroxisomal ß-oxidation in the intestine blunts the effects of neural serotonin signaling on feeding and egg-laying behaviors. Comparative genomics and metabolomics revealed that interfering with intestinal peroxisomal ß-oxidation results in a modest global transcriptional change but significant changes to the metabolome, including a large number of changes in ascaroside and phospholipid species, some of which affect feeding behavior. We also identify body cavity neurons and an ether-a-go-go (EAG)-related potassium channel that functions in these neurons as key cellular components of the circuitry linking peripheral metabolic signals to regulation of neural serotonin signaling. These data raise the possibility that the effects of serotonin on satiety may have their origins in feedback, homeostatic metabolic responses from the periphery.


Subject(s)
Acyl Coenzyme A/metabolism , Feeding Behavior/physiology , Serotonin/metabolism , Animals , Caenorhabditis elegans/metabolism , Caenorhabditis elegans Proteins/metabolism , Fatty Acids/metabolism , Feedback , Homeostasis , Intestines/physiology , Neurons/metabolism , Oxidation-Reduction , Peroxisomes/metabolism , Signal Transduction
3.
PLoS Genet ; 10(6): e1004394, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24921650

ABSTRACT

AMP-activated protein kinase (AMPK) is an evolutionarily conserved master regulator of metabolism and a therapeutic target in type 2 diabetes. As an energy sensor, AMPK activity is responsive to both metabolic inputs, for instance the ratio of AMP to ATP, and numerous hormonal cues. As in mammals, each of two genes, aak-1 and aak-2, encode for the catalytic subunit of AMPK in C. elegans. Here we show that in C. elegans loss of aak-2 mimics the effects of elevated serotonin signaling on fat reduction, slowed movement, and promoting exit from dauer arrest. Reconstitution of aak-2 in only the nervous system restored wild type fat levels and movement rate to aak-2 mutants and reconstitution in only the ASI neurons was sufficient to significantly restore dauer maintenance to the mutant animals. As in elevated serotonin signaling, inactivation of AAK-2 in the ASI neurons caused enhanced secretion of dense core vesicles from these neurons. The ASI neurons are the site of production of the DAF-7 TGF-ß ligand and the DAF-28 insulin, both of which are secreted by dense core vesicles and play critical roles in whether animals stay in dauer or undergo reproductive development. These findings show that elevated levels of serotonin promote enhanced secretions of systemic regulators of pro-growth and differentiation pathways through inactivation of AAK-2. As such, AMPK is not only a recipient of hormonal signals but can also be an upstream regulator. Our data suggest that some of the physiological phenotypes previously attributed to peripheral AAK-2 activity on metabolic targets may instead be due to the role of this kinase in neural serotonin signaling.


Subject(s)
AMP-Activated Protein Kinases/genetics , Caenorhabditis elegans Proteins/genetics , Caenorhabditis elegans/enzymology , Lipid Metabolism/genetics , Nervous System/enzymology , Protein Serine-Threonine Kinases/genetics , Serotonin/metabolism , Animals , Animals, Genetically Modified , Caenorhabditis elegans/genetics , Caenorhabditis elegans Proteins/biosynthesis , Energy Metabolism/genetics , Food , Gene Expression Regulation, Developmental , Genes, Helminth/genetics , Insulins , Lipids/biosynthesis , Longevity/genetics , Nervous System/cytology , RNA Interference , RNA, Small Interfering , Receptor, Insulin/biosynthesis , Secretory Vesicles/metabolism , Transforming Growth Factor beta/biosynthesis , Tryptophan Hydroxylase/genetics
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