Antidiabetic activity of Berberis brandisiana is possibly mediated through modulation of insulin signaling pathway, inflammatory cytokines and adipocytokines in high fat diet and streptozotocin-administered rats DOI Creative Commons

Shumaila Mehdi,

Malik Hassan Mehmood,

Mobeen Ghulam Ahmed

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: April 6, 2023

Medicinal plants play a key role in protection of chronic non-communicable ailments like diabetes, hypertension and dyslipidemia. Berberis brandisiana Ahrendt (Berberidaceae) is traditionally used to treat liver problems, wounds, arthritis, infections, swelling tumors. It also known be enriched with multiple phytoconstituents including berbamine, berberine, quercetin, gallic acid, caffeic vanillic benzoic chlorogenic syringic p-coumaric m-coumaric acid ferulic acid. The efficacy B. has not been established yet diabetes. This study planned assess the antidiabetic activity high fat diet streptozotocin (HFD/STZ)-induced diabetes using animals. Administration aqueous methanolic extract (AMEBB) berbamine (Berb) for 8 weeks caused dose dependent marked (p < 0.01) rise serum insulin HDL levels significant decline glucose, triglycerides, glycosylated hemoglobin (HbA1c), cholesterol, LDL, LFTs RFTs when compared only HFD/STZ-administered rats. AMEBB Berb modulated inflammatory biomarkers (TNF-α, IL-6) adipocytokines (leptin, adiponectin chemerin). (150 mg/kg 300 mg/kg) (80 160 treated rats showed increase 0.001) catalase (Units/mg) pancreas (42.4 ± 0.24, 47.4 0.51), (38.2 0.583, 48.6 1.03) (52 1.41, 63.2 (57.2 0.58, 61.6 1.24) superoxide dismutase (34.8 1.46, 38.2 0.58), (33.2 0.80, 40.4 1.96) (31.8 1.52, 36.8 0.96), (30 0.70, 38.4 0.81),respectively while decrease melondialdehyde (nmol/g) (7.34 0.17, 6.22 0.22), 0.20, 6.34 0.11) (9.08 0.31,8.18 0.29), (9.34 0.10, 8.86 0.24) data HFD/STZ-fed Histopathological studies pancreas, liver, kidney, heart aorta revealed restoration normal tissue architect When mRNA expressions candidate genes were assessed, upregulation IRS-1, SIRT1, GLUT-4 downregulation ADAM17. These findings suggest that possess activity, possibly due its effect on oxidative stress, glucose metabolism, levels. Further ADAM17, demonstrated potential impact homeostasis, resistance markers. Thus, this provides support medicinal use

Language: Английский

Environmental/lifestyle factors in the pathogenesis and prevention of type 2 diabetes DOI Creative Commons
Hubert Kolb, Stéphan Martin

BMC Medicine, Journal Year: 2017, Volume and Issue: 15(1)

Published: July 4, 2017

Environmental and lifestyle changes, in addition to the ageing of populations, are generally believed account for rapid global increase type 2 diabetes prevalence incidence recent decades. In this review, we present a comprehensive overview factors contributing risk, including aspects diet quality quantity, little physical activity, increased monitor viewing time or sitting general, exposure noise fine dust, short disturbed sleep, smoking, stress depression, low socioeconomic status. these promote an body mass index. Since loss β-cell function is ultimate cause developing overt diabetes, environmental changes must have resulted higher risk damage those at genetic risk. Multiple mechanistic pathways may come into play. Strategies prevention should aim promoting 'diabetes-protective lifestyle' whilst simultaneously enhancing resistance human organism pro-diabetic factors. More research on diabetes-protective mechanisms seems warranted.

Language: Английский

Citations

593
Gut microbiota‐derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity DOI
Lars‐Georg Hersoug, Pia Krause Møller, Steffen Loft

et al.

Obesity Reviews, Journal Year: 2015, Volume and Issue: 17(4), P. 297 - 312

Published: Dec. 29, 2015

Summary The composition of the gut microbiota and excessive ingestion high‐fat diets (HFD) are considered to be important factors for development obesity. In this review we describe a coherent mechanism action obesity, which involves microbiota, HFD, low‐grade inflammation, expression fat translocase scavenger receptor CD36, class B type 1 (SR‐BI). SR‐BI binds both lipids lipopolysaccharide (LPS) from Gram‐negative bacteria, may promote incorporation LPS in chylomicrons (CMs). These CMs transported via lymph circulation, where is transferred other lipoproteins by translocases, preferentially HDL. increases binding, transcytosis over endothelial barrier,and endocytosis adipocytes. Especially large size adipocytes with high metabolic activity absorb LPS‐rich lipoproteins. addition, macrophages adipose tissue internalize LPS‐lipoproteins. This contribute polarization M2 M1 phenotype, consequence increased delivery into during hypertrophy. conclusion, evidence suggests that involved obesity as direct targeting molecule lipid storage tissue.

Language: Английский

Citations

255
Antidiabetic agents: Potential anti-inflammatory activity beyond glucose control DOI
André Scheen, Nathalie Esser,

Nicolas Paquot

et al.

Diabetes & Metabolism, Journal Year: 2015, Volume and Issue: 41(3), P. 183 - 194

Published: March 25, 2015

Language: Английский

Citations

138
C-Type Lectin-Like Receptors: Head or Tail in Cell Death Immunity DOI Creative Commons
Marion Drouin, Javier Saenz, Elise Chiffoleau

et al.

Frontiers in Immunology, Journal Year: 2020, Volume and Issue: 11

Published: Feb. 18, 2020

C-type lectin-like receptors (CLRs) represent a family of transmembrane pattern recognition receptors, expressed primarily by myeloid cells. They recognize not only pathogen moieties for host defense, but also modified self-antigens such as damage-associated molecular patterns released from dead Upon ligation, CLR signaling leads to the production inflammatory mediators shape amplitude, duration and outcome immune response. Thus, following excessive injury, dysregulation these development diseases. Herein, we will focus on four CLRs "Dectin family", shown decode immunogenicity cell death. CLEC9A dendritic cells links F-actin exposed dying favor cross-presentation dead-cell associated antigens CD8+ T Nevertheless, exerts feedback mechanisms temper neutrophil recruitment prevent additional tissue damage. MINCLE macrophages binds nuclear SAP130 necrotic potentiate pro-inflammatory responses. However, consequent inflammation can exacerbate pathogenesis Moreover, in tumor microenvironment, induces macrophage-induced suppression cancer progression. Similarly, triggering LOX-1 oxidized LDL, amplifies response promotes escape metastasis. Finally, CLEC12A that recognizes monosodium urate crystals formed during death, inhibits activating signals detrimental inflammation. Interestingly, sustains type-I IFN finely tune responses case viral-induced collateral Therefore, acting concert sensors could be used targeted way treat numerous diseases allergies, obesity, tumors autoimmunity.

Language: Английский

Citations

101
Insulin translates unfavourable lifestyle into obesity DOI Creative Commons
Hubert Kolb, Michael Stümvoll,

Werner Kramer

et al.

BMC Medicine, Journal Year: 2018, Volume and Issue: 16(1)

Published: Dec. 1, 2018

Lifestyle factors conferring increased diabetes risk are associated with elevated basal insulin levels (hyperinsulinaemia). The latter predicts later obesity in children and adolescents. A causal role of hyperinsulinaemia for adipose tissue growth is probable because pharmacological reduction secretion lowers body weight people who obese. Genetic inactivation gene alleles mice also their systemic prevents or ameliorates high-fat diet-induced obesity. Hyperinsulinaemia causes gain a physiological property insulin. Insulin that on the high side normal, which slightly elevated, sufficient to suppress lipolysis promote lipogenesis adipocytes. effect glucose transport hepatic production requires six two times higher hormone levels, respectively. It seems justified suggest lifestyle avoids order limit anabolic fat activity.

Language: Английский

Citations

89
Triglyceride and Triglyceride-Rich Lipoproteins in Atherosclerosis DOI Creative Commons
Baihui Zhang, Fan Yin, Yanan Qiao

et al.

Frontiers in Molecular Biosciences, Journal Year: 2022, Volume and Issue: 9

Published: May 25, 2022

Cardiovascular disease (CVD) is still the leading cause of death globally, and atherosclerosis main pathological basis CVDs. Low-density lipoprotein cholesterol (LDL-C) a strong causal factor atherosclerosis. However, first-line lipid-lowering drugs, statins, only reduce approximately 30% CVD risk. Of note, atherosclerotic (ASCVD) cannot be eliminated in great number patients even their LDL-C levels meet recommended clinical goals. Previously, whether elevated plasma level triglyceride causally associated with ASCVD has been controversial. Recent genetic epidemiological studies have demonstrated that triglyceride-rich (TGRL) are risk factors residual ASCVD. TGRLs metabolites can promote via modulating inflammation, oxidative stress, formation foam cells. In this article, we will make short review TG TGRL metabolism, display evidence association between ASCVD, summarize atherogenic metabolites, discuss current findings advances TG-lowering therapies. This provides information useful for researchers field as well pharmacologists clinicians.

Language: Английский

Citations

40
Dyslipidemia in Patients with Chronic Kidney Disease: An Updated Overview DOI Creative Commons
Sang Heon Suh, Soo Wan Kim

Diabetes & Metabolism Journal, Journal Year: 2023, Volume and Issue: 47(5), P. 612 - 629

Published: Sept. 26, 2023

Dyslipidemia is a potentially modifiable cardiovascular risk factor. Whereas the recommendations for treatment target of dyslipidemia in general population are being more and rigorous, 2013 Kidney Disease: Improving Global Outcomes clinical practice guideline lipid management chronic kidney disease (CKD) presented relatively conservative approach with respect to indication lowering therapy therapeutic monitoring among patients CKD. This may be largely attributed lack high-quality evidence derived from CKD population, whom overall feature considerably distinctive that population. In this review article, we cover characteristic features impact on outcomes We also current modify events finally discuss association between progression potential strategy delay relation therapy.

Language: Английский

Citations

37
Interleukin-1 signaling contributes to acute islet compensation DOI Open Access

Catherine Hajmrle,

Nancy Smith, Aliya F Spigelman

et al.

JCI Insight, Journal Year: 2016, Volume and Issue: 1(4)

Published: April 6, 2016

IL-1β is a well-established inducer of both insulin resistance and impaired pancreatic islet function. Despite this, findings examining IL-1 receptor deficiency or antagonism in vivo animal models, as well clinical studies type 2 diabetic (T2D) patients, have led to conflicting results, suggesting that the actions on glycemic control may be pleiotropic nature. In present work, we find ability amplify glucose-stimulated secretion from human islets correlates with donor BMI. Islets obese donors are sensitized insulinotropic effects this cytokine, whereas stimulatory lost T2D role for signaling compensation. Indeed, mice deficient I become glucose intolerant more rapidly than their WT littermates secretory responses during acute stages inflammatory metabolic stress induced by LPS high-fat diet, respectively. directly enhances β cell increasing granule docking soluble N-ethylmaleimide-sensitive factor attachment (SNARE) complex formation at plasma membrane. Together, our study highlights importance compensation stress.

Language: Английский

Citations

77
Impairment of lysophospholipid metabolism in obesity: altered plasma profile and desensitization to the modulatory properties of n–3 polyunsaturated fatty acids in a randomized controlled trial DOI Creative Commons
Josep M Del Bas-Prior, Antoni Caimari,

M. Isabel Rodriguez-Naranjo

et al.

American Journal of Clinical Nutrition, Journal Year: 2016, Volume and Issue: 104(2), P. 266 - 279

Published: June 16, 2016

Language: Английский

Citations

70
Meal-induced inflammation: postprandial insights from the Personalised REsponses to DIetary Composition Trial (PREDICT) study in 1000 participants DOI Creative Commons
Mohsen Mazidi, Ana M. Valdes, José M. Ordovás

et al.

American Journal of Clinical Nutrition, Journal Year: 2021, Volume and Issue: 114(3), P. 1028 - 1038

Published: April 1, 2021

Meal-induced metabolic changes trigger an acute inflammatory response, contributing to chronic inflammation and associated diseases. We aimed characterize variability in postprandial responses using traditional (IL-6) novel [glycoprotein acetylation (GlycA)] biomarkers of dissect their biological determinants with a focus on glycemia lipemia. Postprandial (0–6 h) glucose, triglyceride (TG), IL-6, GlycA were measured at multiple intervals after sequential mixed-nutrient meals (0 h 4 1002 healthy adults aged 18–65 y from the PREDICT (Personalised REsponses DIetary Composition Trial) 1 study, single-arm dietary intervention study. Measures habitual diet, blood biochemistry, gut microbiome composition, visceral fat mass (VFM) also collected. The IL-6 concentrations highly variable between individuals. Participants eliciting increase (60% 94% total participants, respectively) had mean 6-h increases 11% 190%, respectively. Peak TG glucose significantly (r = 0.83 r 0.24, respectively; both P < 0.001) but not (both > 0.26). A random forest model revealed maximum concentration was strongest predictor structural equation modeling that VFM fasting most strongly GlycA. Network Mendelian randomization demonstrated causal link GlycA, mediated (28%) by TG. Individuals enhanced higher predicted cardiovascular disease risk (using atherosclerotic score) than rest cohort. associations metabolism highlight importance modulating concert obesity reduce low-grade inflammation–related This trial registered clinicaltrials.gov as NCT03479866.

Language: Английский

Citations

54