The Brain-insulin Connection, Metabolic Diseases and Related Pathologies

2010 ◽  
pp. 21-42 ◽  
Author(s):  
Kyriaki Gerozissis
Keyword(s):  
Metabolic Diseases ◽  
Brain Insulin ◽  
The Brain

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 GENETIC DISORDER ALZHEIMER

2017 ◽  
Vol 10 (12) ◽  
pp. 36
Author(s):  
Pratibha Rani ◽  
Kamaldeep Singh ◽  
Anania Arjuna ◽  
Savita Devi
Keyword(s):  
Genetic Factors ◽  
Metabolic Diseases ◽  
Genetic Disorder ◽  
Memory Loss ◽  
Amyloid Plaque ◽  
Specific Protein ◽  
Inhibitor Molecule ◽  
Common Sign ◽  
A Chain ◽  
The Brain

Alzheimer’s disease (AD), slowly continuous neurological disorder, mostly appears in older >65 age that deals with the memory loss due to death or damage of brain cells and cognitive functions (thinking, reasoning, and behavior abnormalities) due to the accumulation of the specific protein (beta-amyloid protein) which form plaque and fibers (tau tangles) in the brain. Not only the genetic factors are responsible but also most of the non-genetic factors are responsible for AD. Several mutations in the gene (APP, APOE, PENS1, PENS2 on chromosome no. 21, 19, 14, 1) are responsible for causing four types of AD. Memory loss is most common sign of AD. Predisposing factors of AD are hereditary, severe brain injury or traumatic, and metabolic diseases such as diabetes mellitus, hypercholesteremia, and obesity. Although treatment can manage some symptoms in few people, but there is no current mechanism to cure AD or stop its progression. Beta-secretase inhibitor molecule prevents the first step in a chain accumulation which leads to the formation of amyloid plaque in the brain. However, the scientist or researchers have established a compound NIC5-15 they have been found NIC5-15 has safe and effectual treatment which has been used to stabilize cognitive performance in patients with mild to moderate AD.

scholarly journals Glucocorticoid receptor action in metabolic and neuronal function

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 1208 ◽  
Author(s):  
Michael J. Garabedian ◽  
Charles A. Harris ◽  
Freddy Jeanneteau
Keyword(s):  
Gene Expression ◽  
Glucocorticoid Receptor ◽  
Metabolic Diseases ◽  
Cell Types ◽  
Health And Disease ◽  
And Behavior ◽  
External Signals ◽  
The Brain

Glucocorticoids via the glucocorticoid receptor (GR) have effects on a variety of cell types, eliciting important physiological responses via changes in gene expression and signaling. Although decades of research have illuminated the mechanism of how this important steroid receptor controls gene expression using in vitro and cell culture–based approaches, how GR responds to changes in external signals in vivo under normal and pathological conditions remains elusive. The goal of this review is to highlight recent work on GR action in fat cells and liver to affect metabolism in vivo and the role GR ligands and receptor phosphorylation play in calibrating signaling outputs by GR in the brain in health and disease. We also suggest that both the brain and fat tissue communicate to affect physiology and behavior and that understanding this “brain-fat axis” will enable a more complete understanding of metabolic diseases and inform new ways to target them.

scholarly journals The Implication of the Brain Insulin Receptor in Late Onset Alzheimer’s Disease Dementia

2018 ◽  
Vol 11 (1) ◽  
pp. 11 ◽  
Author(s):  
Jaume Folch ◽  
Miren Ettcheto ◽  
Oriol Busquets ◽  
Elena Sánchez-López ◽  
Rubén Castro-Torres ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Insulin Receptor ◽  
Late Onset ◽  
Brain Insulin ◽  
The Brain ◽  
Alzheimer’S Disease Dementia

scholarly journals Regulation of brain insulin signaling: A new function for tau

2017 ◽  
Vol 214 (8) ◽  
pp. 2171-2173 ◽  
Author(s):  
Maud Gratuze ◽  
Emmanuel Planel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Insulin Signaling ◽  
Loss Of Function ◽  
Brain Insulin ◽  
The Brain

In this issue of JEM, Marciniak et al. (https://doi.org/10.1084/jem.20161731) identify a putative novel function of tau protein as a regulator of insulin signaling in the brain. They find that tau deletion impairs hippocampal response to insulin through IRS-1 and PTEN dysregulation and suggest that, in Alzheimer’s disease, impairment of brain insulin signaling might occur via tau loss of function.

scholarly journals Fibroblast Growth Factor 21 (FGF21) creates sugar-specific taste aversion to fructose through action in the brain in mice

2020 ◽  
Author(s):  
Darko M. Stevanovic ◽  
Alex J. Hebert ◽  
Bhavna N. Desai ◽  
Garima Singhal ◽  
Andrew C. Adams ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Taste Aversion ◽  
Metabolic Diseases ◽  
Sucrose Preference ◽  
Fibroblast Growth Factor 21 ◽  
List Type ◽  
Fibroblast Growth ◽  
Simple Carbohydrates ◽  
The Brain

AbstractMetabolic diseases such as diabetes and obesity are a growing healthcare concern, and their increasing rates are attributed to increased consumption of carbohydrate-rich diets and sugar-sweetened beverages. Fibroblast growth factor 21 (FGF21) is a complex metabolic regulator, and there is significant evidence that it may play a role in fructose metabolism, driving relative aversion to sweet taste. As such, we examined the relationship between FGF21 and the preferential intake of simple carbohydrates in mice, both as liquid solutions and as dietary additives. Genetic deletion of FGF21 or its obligate co-receptor β-klotho (KLB) had no impact on preference for sugar sweetened solutions. FGF21 overexpression, however, substantially suppressed preference for fructose solutions, but had no effect on glucose or sucrose preference. Infusions of FGF21 also suppressed fructose preference specifically, an effect that was dependent on expression of KLB in the CNS. These results demonstrate that FGF21 creates sugar-specific taste aversion to fructose, which may be mediated by a KLB-dependent pathway in the brain.HighlightsFGF21 administration suppresses fructose preference in mice.Preference for glucose or sucrose is not affected by FGF21 administration.Genetic FGF21 deletion does not enhance fructose, glucose, or sucrose preference.FGF21 requires central β-klotho expression to suppress fructose preference.

scholarly journals Neuropathy and neural plasticity in the subcutaneous white adipose depot

2018 ◽  
Author(s):  
Magdalena Blaszkiewicz ◽  
Jake W. Willows ◽  
Amanda L. Dubois ◽  
Stephen Waible ◽  
Cory P. Johnson ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Neural Plasticity ◽  
Neurotrophic Factor ◽  
Metabolic Diseases ◽  
Metabolic Health ◽  
The Body ◽  
Adipose Tissues ◽  
Adipose Organ ◽  
Tissue Aging ◽  
The Brain

AbstractThe difficulty in obtaining as well as maintaining weight loss, together with the loss of metabolic control in conditions like diabetes and cardiovascular disease, may represent pathological situations of inadequate neural communication between the brain and peripheral organs and tissues. Innervation of adipose tissues by peripheral nerves provides a means of communication between the master metabolic regulator in the brain (chiefly the hypothalamus), and energy-expending and energy-storing cells in the body (primarily adipocytes). Although chemical and surgical denervation studies have clearly demonstrated how crucial adipose tissue neural innervation is for maintaining proper metabolic health, we have uncovered that adipose tissue becomes neuropathic in various conditions of metabolic dysregulation. Here, utilizing both human and mouse adipose tissues, we present evidence of adipose tissue neuropathy, or loss of innervation, under pathophysiological conditions such as obesity, diabetes, and aging, all of which are concomitant with insult to the adipose organ and metabolic dysfunction. Neuropathy is indicated by loss of nerve fiber protein expression, reduction in synaptic markers, and less neurotrophic factor expression in adipose tissue. Aging-related adipose neuropathy particularly results in loss of innervation around the tissue vasculature. These findings underscore that peripheral neuropathy is not restricted to classic tissues like the skin of distal extremities, and that loss of innervation to adipose may trigger or exacerbate metabolic diseases. In addition, we have demonstrated stimulation of adipose tissue neural plasticity with exercise, cold exposure or neurotrophic factor treatment, which may ameliorate adipose neuropathy and be a potential therapeutic option to re-innervate adipose and restore metabolic health.

scholarly journals Targetable Pathways for Alleviating Mitochondrial Dysfunction in Neurodegeneration of Metabolic and Non-Metabolic Diseases

2021 ◽  
Vol 22 (21) ◽  
pp. 11444
Author(s):  
Lauren Elizabeth Millichap ◽  
Elisabetta Damiani ◽  
Luca Tiano ◽  
Iain P. Hargreaves
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Metabolic Diseases ◽  
Molecular Pathways ◽  
Metabolic Demand ◽  
Neuronal Function ◽  
Attractive Therapeutic Target ◽  
Nervous System Function ◽  
Key Events ◽  
The Brain

Many neurodegenerative and inherited metabolic diseases frequently compromise nervous system function, and mitochondrial dysfunction and oxidative stress have been implicated as key events leading to neurodegeneration. Mitochondria are essential for neuronal function; however, these organelles are major sources of endogenous reactive oxygen species and are vulnerable targets for oxidative stress-induced damage. The brain is very susceptible to oxidative damage due to its high metabolic demand and low antioxidant defence systems, therefore minimal imbalances in the redox state can result in an oxidative environment that favours tissue damage and activates neuroinflammatory processes. Mitochondrial-associated molecular pathways are often compromised in the pathophysiology of neurodegeneration, including the parkin/PINK1, Nrf2, PGC1α, and PPARγ pathways. Impairments to these signalling pathways consequently effect the removal of dysfunctional mitochondria, which has been suggested as contributing to the development of neurodegeneration. Mitochondrial dysfunction prevention has become an attractive therapeutic target, and there are several molecular pathways that can be pharmacologically targeted to remove damaged mitochondria by inducing mitochondrial biogenesis or mitophagy, as well as increasing the antioxidant capacity of the brain, in order to alleviate mitochondrial dysfunction and prevent the development and progression of neurodegeneration in these disorders. Compounds such as natural polyphenolic compounds, bioactive quinones, and Nrf2 activators have been reported in the literature as novel therapeutic candidates capable of targeting defective mitochondrial pathways in order to improve mitochondrial function and reduce the severity of neurodegeneration in these disorders.

scholarly journals The Logic of Carotid Body Connectivity to the Brain

Physiology ◽  
2019 ◽  
Vol 34 (4) ◽  
pp. 264-282 ◽  
Author(s):  
Tymoteusz Zera ◽  
Davi J. A. Moraes ◽  
Melina P. da Silva ◽  
James P. Fisher ◽  
Julian F. R. Paton
Keyword(s):  
Carotid Body ◽  
Therapeutic Target ◽  
Metabolic Diseases ◽  
Reflex Response ◽  
Differential Modulation ◽  
Glomus Cell ◽  
Distinct Component ◽  
Differential Control ◽  
The Brain

The carotid body has emerged as a therapeutic target for cardio-respiratory-metabolic diseases. With the expansive functions of the chemoreflex, we sought mechanisms to explain differential control of individual responses. We purport a remarkable correlation between phenotype of a chemosensory unit (glomus cell-sensory afferent) with a distinct component of the reflex response. This logic could permit differential modulation of distinct chemoreflex responses, a strategy ideal for therapeutic exploitation.

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