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.

scholarly journals Hyperinsulinemia: A Metabolic Disease, the Quality of Life of its Patients and Treatment

2020 ◽  
pp. 1-2
Author(s):  
Christos P Beretas ◽  
Keyword(s):  
Quality Of Life ◽  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Metabolic Diseases ◽  
The Body ◽  
Polycystic Ovaries ◽  
Metabolic Condition

Hyperinsulinemia is a metabolic condition that occurs mainly in people with increased body weight, which implies an increased body mass index (BMI) and the consequences it can have in long term. Many people suffer from hyperinsulinemia but do not know it, as they ignore their symptoms which are polycystic ovaries, hair loss, difficulty having children, sparse menstruation, etc. Hyperinsulinemia is a metabolic condition due to the fact that the body constantly produces an increased to excessive amount of insulin regardless of the amount of glucose present in the blood. Hyperinsulinemia should not be confused with and directly linked to diabetes, as type 2 diabetes may occur after several years of untreated hyperinsulinemia due to the natural fatigue of the pancreas due to its excessive and uninterrupted production of insulin. Usually people who show symptoms of hyperinsulinemia are predisposed as it can be diagnosed in newborns, it has arisen from other metabolic diseases such as isletoblastoma, liver disease, etc. It can also result from the administration of drugs such as contraceptives where after their cessation the body has returned to normal or unfortunately hyperinsulinemia may remain.

Multifaceted Effects of Intermittent Fasting in the Treatment and Prevention of Diabetes, Cancer and Obesity or Other Chronic Diseases

2021 ◽  
Vol 18 ◽  
Author(s):  
Priti Tagde ◽  
Sandeep Tagde ◽  
Tanima Bhattacharya ◽  
Pooja Tagde ◽  
Rokeya Akter ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Body Mass Index ◽  
Chronic Diseases ◽  
The Body ◽  
Intermittent Fasting ◽  
Treatment And Prevention ◽  
Obesity And Diabetes ◽  
Hormonal Imbalance

Background: Obesity and diabetes are global epidemics that result in a slew of co-morbid illnesses. Both have been linked to an increased risk of hormonal imbalance, cancer, and other significant disorders, which are a concerning trend for cancer rates in the backdrop of rising obesity and diabetes rates worldwide. Around one in ten persons in the United States and Canada have serious illnesses correlated with type 2 diabetes and early death. It is believed that the US economy alone spends $245 billion annually. Lifestyle modification with intermittent fasting protocol and proper diet helps lower the blood glucose level and maintain the body mass index and reduced the inflammation in the body which is the main cause for all chronic diseases. Methods: We searched case series, clinical trials relating to type 2 diabetes, insulin resistance, cancer, thyroid, cardiovascular disease or other inflammatory diseases in response to intermittent fasting in the PubMed, MEDLINE, and Google Scholar databases. Objective: In this review, we focused on intermittent fasting-based approaches that are becoming more widely accepted for improving health and reducing unwanted effects in patients with type 2 diabetes, cancer, cardiovascular disease, neurodegenerative disease, obesity, thyroid, and hormonal imbalance, which are fasting intermittently and whether intermittent fasting may be considered as a non-medicinal therapeutic option for persons suffering from chronic diseases. Conclusion : Intermittent fasting successfully reversed the diabetes, thyroid, high blood pressure, elevated lipid level, and maintained the body mass index along and also studies has shown that it has been followed or instructed for the treatment and prevention of cancer and neurodegenerative diseases with dietary interventions.

Consequences of Dicarbonyl Stress on Skeletal Muscle Proteins in Type 2 Diabetes

2020 ◽  
Vol 21 (9) ◽  
pp. 878-889 ◽  
Author(s):  
Khurshid Ahmad ◽  
Sibhghatulla Shaikh ◽  
Eun Ju Lee ◽  
Yong-Ho Lee ◽  
Inho Choi
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Metabolic Diseases ◽  
Extracellular Proteins ◽  
The Body ◽  
Elevated Concentration ◽  
Skeletal Muscle Insulin Resistance ◽  
Skeletal Muscle Proteins ◽  
The Impact

Skeletal muscle is the largest organ in the body and constitutes almost 40% of body mass. It is also the primary site of insulin-mediated glucose uptake, and skeletal muscle insulin resistance, that is, diminished response to insulin, is characteristic of Type 2 diabetes (T2DM). One of the foremost reasons posited to explain the etiology of T2DM involves the modification of proteins by dicarbonyl stress due to an unbalanced metabolism and accumulations of dicarbonyl metabolites. The elevated concentration of dicarbonyl metabolites (i.e., glyoxal, methylglyoxal, 3-deoxyglucosone) leads to DNA and protein modifications, causing cell/tissue dysfunctions in several metabolic diseases such as T2DM and other age-associated diseases. In this review, we recapitulated reported effects of dicarbonyl stress on skeletal muscle and associated extracellular proteins with emphasis on the impact of T2DM on skeletal muscle and provided a brief introduction to the prevention/inhibition of dicarbonyl stress.

scholarly journals Metaflammation, NLRP3 Inflammasome Obesity and Metabolic Disease

2011 ◽  
Vol 3 (3) ◽  
pp. 168
Author(s):  
Anna Meiliana ◽  
Andi Wijaya
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Nlrp3 Inflammasome ◽  
Metabolic Diseases ◽  
Inflammatory Responses ◽  
Metabolic Stress ◽  
Nutrient Sensing ◽  
Low Grade ◽  
Wide Range

BACKGROUND: Increasing prevalence of obesity gives rise to many problems associated with multiple morbidities, such as diabetes, hypertension, heart disease, sleep apnea and cancer. The mechanism of obesity is very complex, thus its link to various disease is poorly understood. This review highlights important concepts in our understanding of the pathogenesis of obesity and related complications.CONTENT: Many studies have tried to explore the exciting and puzzling links between metabolic homeostasis and inflammatory responses. A form of subclinical, low-grade systemic inflammation is known to be associated with both obesity and chronic disease. This, later called as "metaflammation", refers to metabolically triggered inflammation. The nutrient-sensing pathway and the immune response coordination are facilitated by these molecular sites in order to maintain homeostasis under diverse metabolic and immune conditions. Recent studies have found that the NLRP3 inflammasome during metabolic stress forms a tie linking TXNIP, oxidative stress, and IL-1β production. This provides new opportunities for research and therapy for the disease often described as the next global pandemic: type 2 diabetes mellitus (T2DM).SUMMARY: The crucial role of metaflammation in many complications of obesity shown by the unexpected overlap between inflammatory and metabolic sensors and their downstream tissue responses. Then great interest arose to explore the pathways that integrate nutrient and pathogen sensing, give more understanding in the mechanisms of insulin resistance type 2 diabetes, and other chronic metabolic pathologies. A family of intracellular sensors called NLR family is a critical component of the innate immune system. They can form multiprotein complexes, called inflammasome which is capable of responding to a wide range of stimuli including both microbial and self molecules by activating the cysteine protease caspase-1, leading to processing and secretion of the proinflammatory cytokines IL-1β and IL-18, which play crucial roles in host defense. Inflammasome dysregulation has been linked to some autoinflammatory and metabolic diseases. These provide opportunities to continue to improve our understanding of the nature of metaflammation in the hope of modifying it to prevent and treat diseasese.KEYWORDS: Inflammation, metaflammation, inflammasome, metabolic disease, obesity

scholarly journals Peran Leptin Terhadap Tes Toleransi Glukosa Oral pada Penderita DM Tipe 2

2020 ◽  
Vol 12 (2) ◽  
pp. 753-760
Author(s):  
Catur Ambar Wati
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Metabolic Diseases ◽  
Tolerance Test ◽  
The Body ◽  
Oral Glucose ◽  
Tingling Sensation

Background: DM is a group of metabolic diseases characterized by hyperglycemia that occurs due to abnormal insulin secretion, insulin action, or both. Symptoms that are complained of in diabetes mellitus sufferers are polydipsia, polyuria, polyphagia, weight loss, and tingling sensation. The oral glucose tolerance test is a test used to diagnose DM when the blood glucose level is less firm, during pregnancy, or to screen for DM or TGT. Leptin is a hormone produced by fat cells that regulate fat storage in the body and adjusts hunger to energy expenditure. Objective: to find out more about the role of leptin on TTGO in people with Type 2 diabetes. Methods: using literature studies from both national and international journals to increase knowledge and understanding of the topics discussed by summarizing the discussion topics and comparing the results presented in the article. Results: Leptin on TTGO examination in individuals with impaired glucose tolerance had a greater chance of becoming diabetes mellitus if there was no intervention in their lifestyle. Conclusion: Leptin plays a role in checking TTGO in people with Type 2 diabetes

scholarly journals Distribution and function of glucagon-like peptide 1 (GLP-1) in the digestive tract of mammals and the clinical use of its analogues

2023 ◽  
Vol 76 (07) ◽  
pp. 6374-2023 ◽  
Author(s):  
ALEKSANDRA GÓRSKA ◽  
MARCIN B. ARCISZEWSKI
Keyword(s):  
Type 2 Diabetes ◽  
Food Intake ◽  
Metabolic Diseases ◽  
Biological Effects ◽  
Glucagon Secretion ◽  
The Body ◽  
Reactive Hypoglycemia ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Recently, interest in glucagon-like peptide-1 (GLP-1) and other peptides derived from preproglucagon has increased significantly. GLP-1 is a 30-amino acid peptide hormone produced in L-type enteroendocrine cells as a response to food intake. GLP-1 is rapidly metabolized and inactivated by the dipeptidyl peptidase IV enzyme before the hormone leaves the intestine, which increases the likelihood that GLP-1 action is transmitted through sensory neurons in the intestine and liver through the GLP-1 receptor. The main actions of GLP-1 are to stimulate insulin secretion (i.e. act as incretin hormone) and inhibit glucagon secretion, thus contributing to the reduction of postprandial glucose spikes. GLP-1 also inhibits motility and gastrointestinal secretion, and therefore acts as part of the „small bowel brake” mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. Because of these effects, GLP-1 or GLP-1 receptor agonists are now increasingly used to treat type 2 diabetes. Reduced GLP-1 secretion may contribute to the development of obesity, and excessive secretion may be responsible for postprandial reactive hypoglycemia. The use of GLP-1 agonists opens up new possibilities for the treatment of type 2 diabetes and other metabolic diseases. In the last two decades, many interesting studies covering both the physiological and pathophysiological role of GLP-1 have been published, and our understanding of GLP-1 has broadened significantly. In this review article, we have tried to describe our current understanding of how GLP-1 works as both a peripheral hormone and as a central neurotransmitter in health and disease. We focused on its biological effects on the body and the potential clinical application in relation to current research.

scholarly journals Assessment of obesity and visceral fat in diabetic nephropathy patients

2019 ◽  
Vol 7 (1) ◽  
pp. 72 ◽  
Author(s):  
Kumar Prafull Chandra ◽  
Balaji D. More ◽  
Anju B. More
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Nephropathy ◽  
Muscle Mass ◽  
Body Fat ◽  
Visceral Fat ◽  
The Body ◽  
Fat Percentage ◽  
Mass Percentage ◽  
Obesity And Diabetes

Background: Diabetic nephropathy is one of the most common diabetic microvascular complication that typically develops after 10 years of diabetes diagnosis. The primary aim of this study was to evaluate the prevalence of obesity and visceral fat in Type 2 Diabetes (T2D) cases with nephropathy and without-nephropathy complication.Methods: In this cross-sectional study, diabetic nephropathy was diagnosed on the basis of biochemical tests of urine albumin, serum creatinine, eGFR, BP, and clinical assessment in patients with T2D. The prevalence of diabetic nephropathy estimated and the association between adiposity and diabetic nephropathy in patients T2D was evaluated. Measures of adiposity included body weight, Body Mass Index (BMI), Waist Circumference (WC), body fat percentage, muscle mass percentage and visceral fat percentage. Analysis of variance indicate difference in the various fat analysis parameters in presence and absence of nephropathy. PROC GLM procedure in the SAS Software was used for statistical calculations.Results: A total of 247 patients with type 2 diabetes (mean age 53.46±11.62 years; 39.5% females) were enrolled in this study. The participants were grouped as with Diabetic Nephropathy (DN) 41.60% (N=99) and without Diabetic Nephropathy (NDN) 58.40% (N=139). The comparison of DN and Non-DN groups showed no significant difference in the BMI, body and visceral fat, muscle mass percentage. Conclusions: Irrespective of the nephropathy status the body fat and visceral fat percentage is increased, and the muscle mass percentage is decreased in diabetes patients. As both obesity and diabetes contribute to the development and progression of renal disease, measures should to taken to reduce the body fat.

scholarly journals Coordinated Actions of FXR and LXR in Metabolism: From Pathogenesis to Pharmacological Targets for Type 2 Diabetes

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Lin Ding ◽  
Shuguang Pang ◽  
Yongmei Sun ◽  
Yuling Tian ◽  
Li Yu ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Nuclear Receptors ◽  
Metabolic Pathways ◽  
Recent Progress ◽  
The Body ◽  
Farnesoid X Receptor ◽  
Pharmacological Targets ◽  
Metabolic Regulators

Type 2 diabetes (T2D) is the most prevalent metabolic disease, and many people are suffering from its complications driven by hyperglycaemia and dyslipidaemia. Nuclear receptors (NRs) are ligand-inducible transcription factors that mediate changes to metabolic pathways within the body. As metabolic regulators, the farnesoid X receptor (FXR) and the liver X receptor (LXR) play key roles in the pathogenesis of T2D, which remains to be clarified in detail. Here we review the recent progress concerning the physiological and pathophysiological roles of FXRs and LXRs in the regulation of bile acid, lipid and glucose metabolism and the implications in T2D, taking into account that these two nuclear receptors are potential pharmaceutical targets for the treatment of T2D and its complications.

Research work undertaken in the Inokuchi Laboratory – Chronic inflammation & chronic disease research including diabetes and metabolic diseases.

Impact ◽  
2020 ◽  
Vol 2020 (7) ◽  
pp. 22-24
Author(s):  
Jin-ichi Inokuchi
Keyword(s):  
Type 2 Diabetes ◽  
Chronic Inflammation ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Research Work ◽  
The Body ◽  
Amplification Loop ◽  
Inside Out ◽  
Ganglioside Species

Today, type 2 diabetes is typically treated by lowering sugar in the blood and increasing the sensitivity of muscle cells to insulin. However, novel discoveries could allow future treatments to target the molecular mechanisms in our bodies that generate insulin resistance – effectively preventing the biological chain of events that causes chronic inflammation and disease to initially occur. Professor Jin-ichi Inokuchi heads the Glycopathology Laboratory at Tohoku Medical and Pharmaceutical University, Japan. Situated within the Institute of Molecular Biomembrane and Glycobiology, the Laboratory focuses on gangliosides and their roles in inflammatory cycles. The scientists are particularly interested in GM3 ganglioside species, as their previous research has indicated that the increased presence of anti-inflammatory GM3 species and decreased presence of pro-inflammatory GM3 species have the power to alter inflammatory cycles in the body, thus contributing to chronic inflammation and associated diseases. Recently, Inokuchi and his colleagues' research revealed some interesting insights regarding GM3. Namely, they discovered that GM3 plays an important role in an inflammation amplification loop that affects diseases involving chronic inflammation, such as type 2 diabetes and metabolic diseases closely linked with obesity. 'Collectively, we propose a novel inflammation loop triggered by GM3 molecular species,' asserts Inokuchi. Inokuchi's research provides an avenue for tackling these conditions from the inside out. By focusing on the biological processes involved in these lifestyle-related chronic diseases, it may be possible to treat type 2 diabetes and metabolic diseases more efficiently.

scholarly journals Enteric phageome alternations in Type 2 diabetes disease

2019 ◽  
Author(s):  
Qian Chen ◽  
Xiaojing Ma ◽  
Chong Li ◽  
Yun Shen ◽  
Wei Zhu ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Gut Microbiota ◽  
Community Composition ◽  
Metabolic Diseases ◽  
Fecal Samples ◽  
Variation Trend ◽  
Similar Variation ◽  
Phage Population

Abstract Background Type 2 diabetes (T2D) is a complex metabolic disease and has been proved to involve in the alternation of the gut microbiota. The previous studies primarily focused on the changes in bacteriome while ignoring the phage community composition. The extracellular phages could lyse the host bacteria, and thus influence the microbiota through the positive or negative interactions with bacteria. We investigated the change of extracellular phageome and explored its role in T2D pathogenesis.Results We used a sequencing-based approach to identify the bacteriophage after isolation of VLPs from the fecal samples. We identified 330 phages according to the predicted host bacteria. The phageome characteristics were highly diverse among individuals. In the T2D group, the intestinal phage population is altered and the abundance of 7 identified phages specific to Enterobacteriaceae hosts were found increased markedly. Additionally, the abundance of Enterobacteriaceae bacteria in gut was significantly increased and the systemic LPS elevation was observed in T2D group. Several phage consortia were found to have significant correlations with T2D disease indicators.Conclusions The alteration of bacteriophages predicted to infect Enterobacteriaceae in the gut was observed in this study, which was expected to be a new source of systemic LPS in T2D patients, and may contribute to the pathogenesis of the disease. The data present in this study revealed the similar variation trend in enteric bacteriome and the correlated bacteriophages, which is likely to shed considerable light on overall understanding the interactions between microbiome and metabolic diseases.

Sign in / Sign up

Export Citation Format

Share Document