scholarly journals Pathophysiological mechanisms that alter the autonomic brain-liver communication in metabolic diseases

Endocrinology ◽  
2021 ◽  
Author(s):  
Anisia Silva ◽  
Alexandre Caron
Keyword(s):  
Metabolic Diseases ◽  
Early Event ◽  
Sympathetic Hyperactivity ◽  
Pathophysiological Mechanisms ◽  
Autonomic Dysfunctions ◽  
The Right ◽  
Metabolic Dysfunctions ◽  
The Brain ◽  
Obesogenic Environments

Abstract The brain influences liver metabolism through many neuroendocrine and autonomic mechanisms that have evolved to protect the organism against starvation and hypoglycemia. Unfortunately, what is normally an effective way to prevent death has become dysregulated in modern obesogenic environments, but the pathophysiological mechanisms behind metabolic dyshomeostasis are still unclear. In this Mini-Review, we provide our thoughts regarding obesity and type 2 diabetes as diseases of the autonomic nervous system. We discuss the pathophysiological mechanisms that alter the autonomic brain-liver communication in these diseases, and how they could represent important targets to prevent or treat metabolic dysfunctions. We discuss how sympathetic hyperactivity to the liver may represent an early event in the progression of metabolic diseases and could progressively lead to hepatic neuropathy. We hope that this discussion will inspire and help framing a model on the importance of better understanding the chronology of autonomic dysfunctions in the liver in order to apply the right strategy at the right time.

Combination of Scutellaria baicalensis and Metformin Ameliorates Diet-Induced Metabolic Dysregulation in Mice via the Gut–Liver–Brain Axis

2020 ◽  
Vol 48 (06) ◽  
pp. 1409-1433
Author(s):  
AbuZar Ansari ◽  
Shambhunath Bose ◽  
Soo-Kyoung Lim ◽  
Jing-Hua Wang ◽  
Young-Hee Choi ◽  
...  
Keyword(s):  
Microbial Population ◽  
Metabolic Diseases ◽  
Neuronal Damage ◽  
The Body ◽  
Scutellaria Baicalensis ◽  
Metabolic Markers ◽  
Metabolic Dysregulation ◽  
High Fructose ◽  
The Brain

Scutellaria baicalensis (SB), a herbal medicine, is commonly used to treat metabolic diseases, while Metformin (MF) is a widely used drug for type 2 diabetes. The purpose of this study was to investigate whether co-treatment of SB with MF could produce a potential therapeutic effect on high-fat and high-fructose diet (HFFD)-induced metabolic dysregulation. First, we optimized the dose of SB (100, 200, 400, and 800[Formula: see text]mg/kg) with MF (200[Formula: see text]mg/kg) in HFFD-induced C57BL6J mice. Next, the optimized dose of SB (400[Formula: see text]mg/kg) was co-administered with MF (50, 100, and 200[Formula: see text]mg/kg) in a similar animal model to find the effective combinations of SB and MF. Metabolic markers were determined in serum and tissues using different assays, histology, gene expression, and gut microbial population. The SB and MF co-treatment significantly decreased the body, liver, and VAT weights. The outcome of OGTT was improved, and the fasting insulin, HbA1c, TG, TC, LDL-c, AST, and ALT were decreased, while HDL-c was significantly increased. Histological analyses revealed maintained the integrity of liver, adipose tissue, and intestine prevented lipid accumulation in the liver and intestine and combated neuronal damage in the brain. Importantly, controlled the expression of PPAR[Formula: see text], and IL-6 genes in the liver, and expression of BDNF, Glut1, Glut3, and Glut4 genes in the brain. Treatment-specific gut microbial segregation was observed in the PCA chart. Our findings indicate that SB and MF co-treatment is an effective therapeutic approach for HFFD-induced metabolic dysregulation which is operated through the gut–liver–brain axis.

scholarly journals Immunomodulatory Role of Urolithin A on Metabolic Diseases

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 192
Author(s):  
Ashley Mulcahy Toney ◽  
Darius Fox ◽  
Virginia Chaidez ◽  
Amanda E. Ramer-Tait ◽  
Soonkyu Chung
Keyword(s):  
Ellagic Acid ◽  
Dietary Intervention ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Alcoholic Fatty Liver ◽  
Urolithin A ◽  
Anti Inflammatory ◽  
The Brain

Urolithin A (UroA) is a gut metabolite produced from ellagic acid-containing foods such as pomegranates, berries, and walnuts. UroA is of growing interest due to its therapeutic potential for various metabolic diseases based on immunomodulatory properties. Recent advances in UroA research suggest that UroA administration attenuates inflammation in various tissues, including the brain, adipose, heart, and liver tissues, leading to the potential delay or prevention of the onset of Alzheimer’s disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. In this review, we focus on recent updates of the anti-inflammatory function of UroA and summarize the potential mechanisms by which UroA may help attenuate the onset of diseases in a tissue-specific manner. Therefore, this review aims to shed new insights into UroA as a potent anti-inflammatory molecule to prevent immunometabolic diseases, either by dietary intervention with ellagic acid-rich food or by UroA administration as a new pharmaceutical drug.

scholarly journals Targeting soluble tumor necrosis factor as a potential intervention to lower risk for late-onset Alzheimer’s disease associated with obesity, metabolic syndrome, and type 2 diabetes

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria Elizabeth De Sousa Rodrigues ◽  
Madelyn C. Houser ◽  
Douglas I. Walker ◽  
Dean P. Jones ◽  
Jianjun Chang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Tumor Necrosis Factor ◽  
Therapeutic Intervention ◽  
Lower Risk ◽  
Tumor Necrosis ◽  
Lipocalin 2 ◽  
The Brain ◽  
Obesogenic Environments ◽  
Necrosis Factor

Abstract Background Insulin impairment and inflammation are two features common to type 2 diabetes and Alzheimer’s disease; however, the molecular and signaling interactions underlying this relationship are not well understood. Mounting evidence point to the associations between the disruption of metabolite processing in insulin impairment and neurodegenerative conditions such as Alzheimer’s. Although the brain depends partially on metabolites processed in the periphery, to date, little is known about how soluble tumor necrosis factor signaling (solTNF) impacts integrated peripheral immune and metabolic feedback signals in states of energy overload and insulin insensitivity. Methods C57Bl/6J mice were fed a high-fat high-carbohydrate diet (HFHC) for 14 weeks. The brain-permeant biologic XPro1595® was used to block solTNF-dependent pathways. Metabolic and immune alterations were evaluated in the gut, liver, and brain. Behavioral tests were performed. Untargeted metabolomics was carried out in the plasma and liver. Results HFHC diet promotes central insulin impairment and dysregulation of immune-modulatory gene expressed in the brain. Alteration of metabolites associated with type 2 diabetes and Alzheimer’s such as butanoate, glutamate, biopterin, branched-chain amino acids, purines, and proteoglycan metabolism was observed in HFHC-fed mice. solTNF inhibition ameliorates hepatic metabolic disturbances and hepatic and intestinal lipocalin-2 levels, and decreases insulin impairment in the brain and behavioral deficits associated with HFHC diet. Conclusions Our novel findings suggest that HFHC diet impacts central insulin signaling and immune-metabolic interactions in a solTNF-dependent manner to increase the risk for neurodegenerative conditions. Our novel findings indicate that selective solTNF neutralization can ameliorate peripheral and central diet-induced insulin impairment and identify lipocalin-2 as a potential target for therapeutic intervention to target inflammation and insulin disturbances in obesogenic environments. Collectively, our findings identify solTNF as a potential target for therapeutic intervention in inflammatory states and insulin disturbances in obesogenic environments to lower risk for AD.

The brain structure and neurosecretory cells of noctuid moth Anadevidia peponis: Noctuidae

1990 ◽  
Vol 48 (3) ◽  
pp. 436-437
Author(s):  
M. Sato ◽  
Y. Ogawa ◽  
M. Sasaki ◽  
T. Matsuo
Keyword(s):  
Biological Clock ◽  
Virgin Female ◽  
Basic Structure ◽  
Fixed Time ◽  
Neurosecretory Cells ◽  
Nerve Cells ◽  
Noctuid Moth ◽  
The Right ◽  
20 Nm ◽  
The Brain

A virgin female of the noctuid moth, a kind of noctuidae that eats cucumis, etc. performs calling at a fixed time of each day, depending on the length of a day. The photoreceptors that induce this calling are located around the neurosecretory cells (NSC) in the central portion of the protocerebrum. Besides, it is considered that the female’s biological clock is located also in the cerebral lobe. In order to elucidate the calling and the function of the biological clock, it is necessary to clarify the basic structure of the brain. The observation results of 12 or 30 day-old noctuid moths showed that their brains are basically composed of an outer and an inner portion-neural lamella (about 2.5 μm) of collagen fibril and perineurium cells. Furthermore, nerve cells surround the cerebral lobes, in which NSCs, mushroom bodies, and central nerve cells, etc. are observed. The NSCs are large-sized (20 to 30 μm dia.) cells, which are located in the pons intercerebralis of the head section and at the rear of the mushroom body (two each on the right and left). Furthermore, the cells were classified into two types: one having many free ribosoms 15 to 20 nm in dia. and the other having granules 150 to 350 nm in dia. (Fig. 1).

STUDY OF RADIATION CHARACTERISTICS THE RENAL FUNCTION IN PATIENTS WITH TYPE 2 DIABETES

2014 ◽  
pp. 73-77
Author(s):  
Van Chuong Nguyen ◽  
Thi Kim Anh Nguyen
Keyword(s):  
Type 2 Diabetes ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Disease Duration ◽  
Left Kidney ◽  
Cross Sectional ◽  
The Right

Background: A Research glomerular filtration rate (GFR) of 61 patients with type 2 diabetes mellitus with renal scanning 99mTc-DTPA glomerular filtration rate at the hospital 175. Objective: (1) To study characteristics of imaging of renal function. (2) Understanding the relationship between GFR with blood sugar, HbA1c, blood pressure and albuminuria in patients with type 2 diabetes. Methods: Descriptive, prospective, cross-sectional study. Clinical examination, Clinical tests and 99mTc-DTPA GFR gamma - camera renography for patients. Result: GFR of the study group was 75,4 ± 22,3 ml/phut/1,73m2, the left kidney was 35,0 ± 13,0 is lower than the right kidney and 39,8 ± 11,9; p <0,01. There is no correlation between GFR with blood glucose and HbA1c, the risk of reduced GFR in hypertensive group associated is OR = 6,5 with p<0,01; albuminuria (+) is OR = 4,2 with p <0,01; and disease duration > 10 years is OR = 3,5 with p <0.01. Conclusion: GFR of the left kidneys is lower than the right kidney; correlation decreased GFR associated with hypertension, albuminuria and disease duration. Keywords: GFR, diabetes, albuminuria

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.

ASSESSMENT OF PHYSIOLOGICAL PARAMETERS OF THE TRIGEMINAL AND COCHLEOVESTIBULAR SYSTEMS IN TEMPOROMANDIBULAR JOINT PAIN DYSFUNCTION

2020 ◽  
Vol 17 (2) ◽  
pp. 110-120
Author(s):  
N.D. Sorokina ◽  
◽  
L.R. Shahalieva ◽  
S.S. Pertsov ◽  
L.V. Polma ◽  
...  
Keyword(s):  
Nervous System ◽  
Evoked Potentials ◽  
Temporomandibular Joint ◽  
Differential Diagnostics ◽  
Autonomous Nervous System ◽  
Dental Diseases ◽  
Grade Ii ◽  
The Right ◽  
Distal Occlusion ◽  
The Brain

One of the most common causes of chronic pain in the facial region, including in the trigeminal nerve link, which is not associated with dental diseases, is pain dysfunction of the temporomandibular joint. At the same time, there is evidence in the literature that there are relationships between pain dysfunction of the temporomandibular joint, abnormal occlusion, cervical-muscular tonic phenomena, postural disorders, dysfunction of the Autonomous nervous system and cochleovestibular manifestations. At the same time, neurophysiological indicators of functional disorders in the maxillofacial region and intersystem interactions in pain dysfunction of the temporomandibular joint are insufficiently studied.Goal. The aim of the work is to evaluate the neurophysiological features of trigeminal afferentation in terms of trigeminal somatosensory evoked potentials (TSWP) and the auditory conducting system of the brain in terms of acoustic stem evoked potentials (ASVP) in distal occlusion of the dentition with pain dysfunction of the temporomandibular joint (TMJ) in comparison with physiological occlusion in students 18-21 years old. Material and methods. The main study included 41 students with distal occlusion (21 girls and 20 boys), (grade II Engl, symmetrically right and left in 14 people, and grade II Engl on the left and grade I on the right in 12 people, grade I on the left and grade II on the right in 15 people). All respondents with distal occlusion and who were practically healthy signed an informed consent to participate in the study. We used complex orthodontic methods of examination, subjective degree of severity and intensity of pain in the TMJ, assessment of the Autonomous nervous system (samples and tests), and neurophysiological methods for assessing TSVP and ASVP. Results. Significant differences in ASEP parameters were found in the group of respondents with distal occlusion in the form of a decrease in the latency period of peak I, III, and V compared to physiological occlusion, that correlated with the subjective assessment (in points) of cochleovestibular disorders. According to the TSVP study, a decrease in the duration of latent periods was found, which indicates an increased excitability of non-specific brain stem structures at the medullo-ponto-mesencephalic level compared to the control group. Conclusions. The results obtained are supposed to be used for differential diagnostics, including such dental diseases as TMJ pain dysfunction, occlusion abnormalities accompanied by pain syndrome. Additional functional diagnostics of multi-modal VP of the brain (acoustic evoked potentials, trigeminal evoked potentials) can be performed in conjunction with indicators of autonomic nervous system dysfunction, with parameters of severity of clinical symptoms of cochleovestibular disorders, musculoskeletal dysfunction the maxillofacial area, with indicators of pain, which will determine the tactics and effectiveness of subsequent treatment.

scholarly journals Learning of food preferences: mechanisms and implications for obesity & metabolic diseases

2021 ◽  
Author(s):  
Hans-Rudolf Berthoud ◽  
Christopher D. Morrison ◽  
Karen Ackroff ◽  
Anthony Sclafani
Keyword(s):  
Metabolic Diseases ◽  
Food Preferences ◽  
Reward System ◽  
Nutrient Sensing ◽  
Vagal Afferents ◽  
Dietary Knowledge ◽  
Ongoing Work ◽  
Brain Reward ◽  
The Brain ◽  
Vagal Function

AbstractOmnivores, including rodents and humans, compose their diets from a wide variety of potential foods. Beyond the guidance of a few basic orosensory biases such as attraction to sweet and avoidance of bitter, they have limited innate dietary knowledge and must learn to prefer foods based on their flavors and postoral effects. This review focuses on postoral nutrient sensing and signaling as an essential part of the reward system that shapes preferences for the associated flavors of foods. We discuss the extensive array of sensors in the gastrointestinal system and the vagal pathways conveying information about ingested nutrients to the brain. Earlier studies of vagal contributions were limited by nonselective methods that could not easily distinguish the contributions of subsets of vagal afferents. Recent advances in technique have generated substantial new details on sugar- and fat-responsive signaling pathways. We explain methods for conditioning flavor preferences and their use in evaluating gut–brain communication. The SGLT1 intestinal sugar sensor is important in sugar conditioning; the critical sensors for fat are less certain, though GPR40 and 120 fatty acid sensors have been implicated. Ongoing work points to particular vagal pathways to brain reward areas. An implication for obesity treatment is that bariatric surgery may alter vagal function.

scholarly journals Synergistic Effects of Milk-Derived Exosomes and Galactose on α-Synuclein Pathology in Parkinson’s Disease and Type 2 Diabetes Mellitus

2021 ◽  
Vol 22 (3) ◽  
pp. 1059
Author(s):  
Bodo C. Melnik
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Dopaminergic Neurons ◽  
Vagal Nerve ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
The Brain

Epidemiological studies associate milk consumption with an increased risk of Parkinson’s disease (PD) and type 2 diabetes mellitus (T2D). PD is an α-synucleinopathy associated with mitochondrial dysfunction, oxidative stress, deficient lysosomal clearance of α-synuclein (α-syn) and aggregation of misfolded α-syn. In T2D, α-syn promotes co-aggregation with islet amyloid polypeptide in pancreatic β-cells. Prion-like vagal nerve-mediated propagation of exosomal α-syn from the gut to the brain and pancreatic islets apparently link both pathologies. Exosomes are critical transmitters of α-syn from cell to cell especially under conditions of compromised autophagy. This review provides translational evidence that milk exosomes (MEX) disturb α-syn homeostasis. MEX are taken up by intestinal epithelial cells and accumulate in the brain after oral administration to mice. The potential uptake of MEX miRNA-148a and miRNA-21 by enteroendocrine cells in the gut, dopaminergic neurons in substantia nigra and pancreatic β-cells may enhance miRNA-148a/DNMT1-dependent overexpression of α-syn and impair miRNA-148a/PPARGC1A- and miRNA-21/LAMP2A-dependent autophagy driving both diseases. MiRNA-148a- and galactose-induced mitochondrial oxidative stress activate c-Abl-mediated aggregation of α-syn which is exported by exosome release. Via the vagal nerve and/or systemic exosomes, toxic α-syn may spread to dopaminergic neurons and pancreatic β-cells linking the pathogenesis of PD and T2D.

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