scholarly journals Ecological Sensing Through Taste and Chemosensation Mediates Inflammation: A Biological Anthropological Approach

2020 ◽  
Vol 11 (6) ◽  
pp. 1671-1685 ◽  
Author(s):  
Cristina Giuliani ◽  
Claudio Franceschi ◽  
Donata Luiselli ◽  
Paolo Garagnani ◽  
Stanley Ulijaszek
Keyword(s):  
Niche Construction ◽  
Metabolic Diseases ◽  
Molecular Level ◽  
Taste Perception ◽  
Human Niche Construction ◽  
Inflammatory Processes ◽  
Anthropological Approach ◽  
Interkingdom Communication ◽  
Integrated Responses

ABSTRACT Ecological sensing and inflammation have evolved to ensure optima between organism survival and reproductive success in different and changing environments. At the molecular level, ecological sensing consists of many types of receptors located in different tissues that orchestrate integrated responses (immune, neuroendocrine systems) to external and internal stimuli. This review describes emerging data on taste and chemosensory receptors, proposing them as broad ecological sensors and providing evidence that taste perception is shaped not only according to sense epitopes from nutrients but also in response to highly diverse external and internal stimuli. We apply a biological anthropological approach to examine how ecological sensing has been shaped by these stimuli through human evolution for complex interkingdom communication between a host and pathological and symbiotic bacteria, focusing on population-specific genetic diversity. We then focus on how these sensory receptors play a major role in inflammatory processes that form the basis of many modern common metabolic diseases such as obesity, type 2 diabetes, and aging. The impacts of human niche construction and cultural evolution in shaping environments are described with emphasis on consequent biological responsiveness.

scholarly journals Visfatin Triggers Anorexia and Body Weight Loss through Regulating the Inflammatory Response in the Hypothalamic Microglia

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Thai Hien Tu ◽  
Il Seong Nam-Goong ◽  
Jisung Lee ◽  
Sunggu Yang ◽  
Jae Geun Kim
Keyword(s):  
Body Weight ◽  
Inflammatory Response ◽  
Energy Homeostasis ◽  
Metabolic Diseases ◽  
Body Weight Loss ◽  
Central Administration ◽  
Physiological Processes ◽  
Microglial Cell Line ◽  
Inflammatory Processes

Visfatin is an adipokine that is secreted from adipose tissue, and it is involved in a variety of physiological processes. In particular, visfatin has been implicated in metabolic diseases, such as obesity and type 2 diabetes, which are directly linked to systemic inflammation. However, the potential impacts of visfatin on the hypothalamic control of energy homeostasis, which is involved in microglial inflammation, have not fully been investigated. In this study, we found that treatment with exogenous recombinant visfatin protein led to the activation of the inflammatory response in a microglial cell line. In addition, we observed that central administration of visfatin led to the activation of microglia in the hypothalamus. Finally, we found that visfatin reduced food intake and body weight through activating POMC neurons in association with microglia activation in mice. These findings indicate that elevation of central visfatin levels may be associated with homeostatic feeding behavior in response to metabolic shifts, such as increased adiposity following inflammatory processes in the hypothalamus.

Mutations of mtDNA in some vascular and metabolic diseases

2020 ◽  
Vol 26 ◽  
Author(s):  
Margarita A. Sazonova ◽  
Anastasia I. Ryzhkova ◽  
Vasily V. Sinyov ◽  
Marina D. Sazonova ◽  
Tatiana V. Kirichenko ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Coronary Heart Disease ◽  
Type 2 Diabetes Mellitus ◽  
Heart Disease ◽  
Chronic Diseases ◽  
Metabolic Diseases ◽  
Present Review ◽  
Mtdna Mutations

Background: The present review article considers some chronic diseases of vascular and metabolic genesis, the causes of which may be mitochondrial dysfunction. Very often, in the long course of the disease, complications may occur, leading to myocardial infarction or ischemic stroke and as a result, death.In particular, a large percentage of human deaths nowadays belongs to cardiovascular diseases such as coronary heart disease (CHD), arterial hypertension, cardiomyopathies and type 2 diabetes mellitus. Objective: The aim of the present review was the analysis of literature sources, devoted to an investigation of a link of mitochondrial DNA mutations with chronic diseases of vascular and metabolic genesis, Results: The analysis of literature indicates the association of the mitochondrial genome mutations with coronary heart disease, type 2 diabetes mellitus, hypertension and various types of cardiomyopathies. Conclusion: The detected mutations can be used to analyze the predisposition to chronic diseases of vascular and metabolic genesis. They can also be used to create molecular-cell models necessary to evaluate the effectiveness of drugs developed for treatment of these pathologies. MtDNA mutations associated withthe absence of diseases of vascular and metabolic genesis could be potential candidates for gene therapy of diseases of vascular and metabolic genesis.

scholarly journals Historical Ecology of Scandinavian Infield Systems

2021 ◽  
Vol 13 (2) ◽  
pp. 817
Author(s):  
Ove Eriksson ◽  
Matilda Arnell ◽  
Karl-Johan Lindholm
Keyword(s):  
Middle Ages ◽  
Iron Age ◽  
Historical Ecology ◽  
Niche Construction ◽  
Livestock Grazing ◽  
Land Reforms ◽  
Hay Meadows ◽  
Human Niche Construction ◽  
Major Transition ◽  
The 19Th Century

Infield systems originated during the early Iron Age and existed until the 19th century, although passing many transitions and changes. The core features of infield systems were enclosed infields with hay-meadows and crop fields, and unenclosed outland mainly used for livestock grazing. We examine the transitions and changes of domesticated landscapes with infield systems using the framework of human niche construction, focusing on reciprocal causation affecting change in both culture and environment. A first major transition occurred during the early Middle Ages, as a combined effect of a growing elite society and an increased availability of iron promoted expansion of villages with partly communal infields. A second major transition occurred during the 18th and 19th centuries, due to a then recognized inefficiency of agricultural production, leading to land reforms. In outlands, there was a continuous expansion of management throughout the whole period. Even though external factors had significant impacts as well, human niche construction affected a range of cultural and environmental features regarding the management and structure of domesticated landscapes with infield systems. Thus, niche construction theory is a useful framework for understanding the historical ecology of infield systems.

Immunometabolism of obesity and diabetes: microbiota link compartmentalized immunity in the gut to metabolic tissue inflammation

2015 ◽  
Vol 129 (12) ◽  
pp. 1083-1096 ◽  
Author(s):  
Joseph B. McPhee ◽  
Jonathan D. Schertzer
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Immune Responses ◽  
Metabolic Diseases ◽  
The Body ◽  
Tissue Inflammation ◽  
Gut Barrier Function ◽  
Inflammatory Status ◽  
Obesity And Diabetes

The bacteria that inhabit us have emerged as factors linking immunity and metabolism. Changes in our microbiota can modify obesity and the immune underpinnings of metabolic diseases such as Type 2 diabetes. Obesity coincides with a low-level systemic inflammation, which also manifests within metabolic tissues such as adipose tissue and liver. This metabolic inflammation can promote insulin resistance and dysglycaemia. However, the obesity and metabolic disease-related immune responses that are compartmentalized in the intestinal environment do not necessarily parallel the inflammatory status of metabolic tissues that control blood glucose. In fact, a permissive immune environment in the gut can exacerbate metabolic tissue inflammation. Unravelling these discordant immune responses in different parts of the body and establishing a connection between nutrients, immunity and the microbiota in the gut is a complex challenge. Recent evidence positions the relationship between host gut barrier function, intestinal T cell responses and specific microbes at the crossroads of obesity and inflammation in metabolic disease. A key problem to be addressed is understanding how metabolite, immune or bacterial signals from the gut are relayed and transferred into systemic or metabolic tissue inflammation that can impair insulin action preceding Type 2 diabetes.

Intramyocellular fat storage in metabolic diseases

2016 ◽  
Vol 26 (1) ◽  
Author(s):  
Claire Laurens ◽  
Cedric Moro
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Metabolic Diseases ◽  
Recent Literature ◽  
Lipid Storage ◽  
Muscle Lipid ◽  
The Past ◽  
Skeletal Muscle Lipid ◽  
Ectopic Lipid Storage

AbstractOver the past decades, obesity and its metabolic co-morbidities such as type 2 diabetes (T2D) developed to reach an endemic scale. However, the mechanisms leading to the development of T2D are still poorly understood. One main predictor for T2D seems to be lipid accumulation in “non-adipose” tissues, best known as ectopic lipid storage. A growing body of data suggests that these lipids may play a role in impairing insulin action in metabolic tissues, such as liver and skeletal muscle. This review aims to discuss recent literature linking ectopic lipid storage and insulin resistance, with emphasis on lipid deposition in skeletal muscle. The link between skeletal muscle lipid content and insulin sensitivity, as well as the mechanisms of lipid-induced insulin resistance and potential therapeutic strategies to alleviate lipotoxic lipid pressure in skeletal muscle will be discussed.

scholarly journals Human niche construction in interdisciplinary focus

2011 ◽  
Vol 366 (1566) ◽  
pp. 785-792 ◽  
Author(s):  
Jeremy Kendal ◽  
Jamshid J. Tehrani ◽  
John Odling-Smee
Keyword(s):  
Natural Selection ◽  
Material Culture ◽  
Niche Construction ◽  
Cultural Knowledge ◽  
Causal Process ◽  
Genetic Inheritance ◽  
Selection Pressures ◽  
Ecological Inheritance ◽  
Human Niche Construction ◽  
The Social

Niche construction is an endogenous causal process in evolution, reciprocal to the causal process of natural selection. It works by adding ecological inheritance , comprising the inheritance of natural selection pressures previously modified by niche construction, to genetic inheritance in evolution. Human niche construction modifies selection pressures in environments in ways that affect both human evolution, and the evolution of other species. Human ecological inheritance is exceptionally potent because it includes the social transmission and inheritance of cultural knowledge, and material culture. Human genetic inheritance in combination with human cultural inheritance thus provides a basis for gene–culture coevolution, and multivariate dynamics in cultural evolution. Niche construction theory potentially integrates the biological and social aspects of the human sciences. We elaborate on these processes, and provide brief introductions to each of the papers published in this theme issue.

scholarly journals Mitochondrial Heterogeneity in Metabolic Diseases

Biology ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 927
Author(s):  
Jennifer Ngo ◽  
Corey Osto ◽  
Frankie Villalobos ◽  
Orian S. Shirihai
Keyword(s):  
Metabolic Diseases ◽  
Kidney Diseases ◽  
Pancreatic Beta Cell ◽  
Disease Onset ◽  
Metabolic Signaling ◽  
Isolation Techniques ◽  
Functional Differences ◽  
Architectural Features ◽  
Mitochondrial Heterogeneity

Mitochondria have distinct architectural features and biochemical functions consistent with cell-specific bioenergetic needs. However, as imaging and isolation techniques advance, heterogeneity amongst mitochondria has been observed to occur within the same cell. Moreover, mitochondrial heterogeneity is associated with functional differences in metabolic signaling, fuel utilization, and triglyceride synthesis. These phenotypic associations suggest that mitochondrial subpopulations and heterogeneity influence the risk of metabolic diseases. This review examines the current literature regarding mitochondrial heterogeneity in the pancreatic beta-cell and renal proximal tubules as they exist in the pathological and physiological states; specifically, pathological states of glucolipotoxicity, progression of type 2 diabetes, and kidney diseases. Emphasis will be placed on the benefits of balancing mitochondrial heterogeneity and how the disruption of balancing heterogeneity leads to impaired tissue function and disease onset.

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