scholarly journals Galectin-3 In Obesity And Type 2 Diabetes

2015 ◽  
Vol 16 (4) ◽  
pp. 273-280
Author(s):  
Nada Pejnovic
Keyword(s):  
Metabolic Disease ◽  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Inflammatory Responses ◽  
Current Evidence ◽  
Galectin 3 ◽  
Important Player ◽  
Severe Pathology ◽  
Visceral Adipose

AbstractGalectin-3 is an important regulator of inflammation and acts as a receptor for advanced-glycation (AGE) and lipoxidation end-products (ALE). Evidence indicates a significant upregulation in circulating levels and visceral adipose tissue production of Galectin-3 in obesity and type 2 diabetes. Recent studies demonstrate development of obesity and dysregulation of glucose metabolism in Galectin-3 “knockout” (KO) mice, which also develop accelerated and more severe pathology in models of atherosclerosis and metabolically-induced kidney damage. Thus, evidence that Galectin-3 is an important player in metabolic disease is accumulating. This review discusses current evidence on the connection between Galectin-3 and metabolic disease, focusing on mechanisms by which this galectin modulates adiposity, glucose metabolism and obesity-associated inflammatory responses.

scholarly journals Galectin-3 Deletion Enhances Visceral Adipose Tissue Inflammation and Dysregulates Glucose Metabolism in Mice on a High-Fat Diet

2016 ◽  
Vol 17 (3) ◽  
pp. 231-240 ◽  
Author(s):  
Ilija Jeftic ◽  
Marina Miletic-Kovacevic ◽  
Nemanja Jovicic ◽  
Jelena Pantic ◽  
Nebojsa Arsenijevic ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Galectin 3 ◽  
Visceral Adipose

Abstract Obesity and type 2 diabetes mellitus (T2DM) constitute major health problems worldwide. Increased visceral adiposity enhances the risk of insulin resistance and type 2 diabetes. The mechanisms involved in obesity-associated chronic inflammation in metabolic tissues (metaflammation) that lead to insulin resistance and dysregulated glucose metabolism are incompletely defined. Galectin-3 (Gal-3), a β-galactoside-binding lectin, modulates immune/inflammatory responses and specifically binds to metabolic danger molecules. To dissect the role of Gal-3 in obesity and diabetes, Gal-3-deficient (LGALS3-/-) and wild-type (WT) C57Bl/6 male mice were placed on a high-fat diet (HFD, 60% kcal fat) or a standard chow diet (10% kcal fat) for 6 months and metabolic, histological and immunophenotypical analyses of the visceral adipose tissue were performed. HFD-fed LGALS3-/- mice had higher body weights and more body weight gain, visceral adipose tissue (VAT), hyperglycaemia, hyperinsulinemia, insulin resistance and hyperlipidemia than diet-matched WT mice. Compared to WT mice, the enlarged VAT in obese LGALS3-/- mice contained larger adipocytes. Additionally, we demonstrate enhanced inflammation in the VAT of LGALS3-/- mice compared with diet-matched WT mice. The VAT of LGALS3-/- mice fed a HFD contained more numerous dendritic cells and proinflammatory F4/80+CD11c+CD11b+ and F4/80high macrophages. In contrast to WT mice, the numbers of CXCR3+ and CD8+ T cells were increased in the VAT of Gal-3-deficient mice after 6 months of high-fat feeding. We provide evidence that Gal-3 ablation results in enhanced HFD-induced adiposity, inflammation in the adipose tissue, insulin resistance and hyperglycaemia. Thus, Gal-3 represents an important regulator of obesity-associated immunometabolic alterations.

scholarly journals Evidence and Potential Mechanisms of Jin-Gui Shen-Qi Wan as a Treatment for Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhipeng Hu ◽  
Xiaoke Liu ◽  
Maoyi Yang
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Combination Treatment ◽  
Meta Analysis ◽  
Hypoglycemic Agents ◽  
Current Evidence

Background: Type 2 diabetes mellitus (T2DM) is a subtype of diabetes mellitus characterized by progressive dysfunction of β-cell insulin secretion and insulin resistance. Jīn-Guì Shèn-Qì Wán (JGSQW) has for many years been widely used in clinical practice as a treatment for T2DM. However, its effect remains unknown.Objectives: This study aims to summarize the clinical evidence of the effect of JGSQW on glucose and lipid metabolism in T2DM and the potential mechanisms underlying this effect.Methods: Six databases were searched without language or publication status restrictions. Data were extracted to a predefined template for synthesis.Results: Fourteen studies with 1586 participants were included in this meta-analysis. All 14 studies were judged to be at high risk of bias. JGSQW is safe for T2DM patients. Pooled results indicated that combination treatment results in a reduction in glycated hemoglobin (HbA1c) (mean difference (MD) −0.49%; 95% CI −0.67 to −0.31), fasting blood glucose (FBG) (MD −0.84; 95% CI −1.19 to −0.49), and 2-hour postprandial glucose 2hBG (MD −1.38; 95% CI −1.60 to −1.16). No significant difference in glucose metabolism was observed between JGSQW and hypoglycemic agents. The available evidence was insufficient to determine the effects on lipid metabolism. Sensitivity analyses indicated that these results were robust.Conclusion: By combining the available evidence, we found that JGSQW is safe for T2DM patients. Compared with hypoglycemic agents alone, combination treatment with JGSQW enhances the effect on glucose metabolism in patients with T2DM. We found no difference in the efficacy of JGSQW alone compared to hypoglycemic agents alone. In terms of lipid metabolism, the current evidence is insufficient and too inconsistent for us to draw firm conclusions, so further studies are needed.

scholarly journals Type 2 Diabetes and Dietary Carbohydrate Intake of Adolescents and Young Adults: What Is the Impact of Different Choices?

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3344
Author(s):  
Luisa Bonsembiante ◽  
Giovanni Targher ◽  
Claudio Maffeis
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Harmful Effect ◽  
Current Evidence ◽  
Single Individual ◽  
Glycemic Response ◽  
Dietary Carbohydrates ◽  
High Consumption ◽  
The Impact

Type 2 diabetes mellitus has a high prevalence worldwide, with a rapidly increasing incidence even in youth. Nutrition, dietary macronutrient composition, and in particular dietary carbohydrates play a major role in the development of type 2 diabetes. The aim of this narrative review is to discuss the current evidence on the role of dietary carbohydrates in the prevention and management of type 2 diabetes. The digestibility or availability of carbohydrates and their glycemic index (and glycemic load) markedly influence the glycemic response. High consumption of dietary fiber is beneficial for management of type 2 diabetes, whereas high consumption of both glycemic starch and sugars may have a harmful effect on glucose metabolism, thereby increasing the risk of developing type 2 diabetes in the presence of genetic predisposition or making its glycemic control more difficult to achieve in people with established T2D. Therefore, the same dietary macronutrient may have harmful or beneficial effects on type 2 diabetes mainly depending on the subtypes consumed. Some other factors are involved in glucose metabolism, such as meal composition, gut microbiota and genetics. For this reason, the glycemic response after carbohydrate consumption is not easy to predict in the single individual. Nutrition suggested to subjects with known type 2 diabetes should be always person-centered, considering the individual features of each subject.

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

Plasma Mir-193b-3p Is Elevated in Type 2 Diabetes and Could Impair Glucose Metabolism

2019 ◽  
Author(s):  
Hua Hu ◽  
Meng Zhao ◽  
Zhaoyang Li ◽  
Hongli Nie ◽  
Jia He ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism

Liraglutide Therapy in a Prediabetic State: Rethinking the Evidence

2020 ◽  
Vol 16 (7) ◽  
pp. 699-715 ◽  
Author(s):  
Georgios S. Papaetis
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Glucose Tolerance ◽  
Current Evidence ◽  
Β Cell ◽  
Prediabetic State ◽  
New Therapeutic Approaches ◽  
Normal Glucose

Background: Prediabetes is defined as a state of glucose metabolism between normal glucose tolerance and type 2 diabetes. Continuous β-cell failure and death are the reasons for the evolution from normal glucose tolerance to prediabetes and finally type 2 diabetes. Introduction: The necessity of new therapeutic approaches in order to prevent or delay the development of type 2 diabetes is obligatory. Liraglutide, a long-acting GLP-1 receptor agonist, has 97% homology for native GLP-1. Identification of the trophic and antiapoptotic properties of liraglutide in preclinical studies, together with evidence of sustained β-cell function longevity during its administration in type 2 diabetes individuals, indicated its earliest possible administration during this disease, or even before its development, so as to postpone or delay its onset. Methods: Pubmed and Google databases have been thoroughly searched and relevant studies were selected. Results: This paper explores the current evidence of liraglutide administration both in humans and animal models with prediabetes. Also, it investigates the safety profile of liraglutide treatment and its future role to postpone or delay the evolution of type 2 diabetes. Conclusion: Liralgutide remains a valuable tool in our therapeutic armamentarium for individuals who are overweight or obese and have prediabetes. Future well designed studies will give valuable information that will help clinicians to stratify individuals who will derive the most benefit from this agent, achieving targeted therapeutic strategies.

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