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Sex-specific and dose-response relationships of urinary cobalt and molybdenum levels with glucose levels and Insulin resistance in U.S. adults

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Journal of Environmental Sciences 2023年第2期124卷 42-49页

作者： Jingli Yang Yongbin Lu Yana Bai Zhiyuan Cheng College of Earth and Environmental Sciences Lanzhou UniversityLanzhou 730000China Department of Epidemiology and Statistics School of Public HealthLanzhou UniversityLanzhou 730000China School of Public Health and Emergency Management Southern University of Science and TechnologyShenzhen 518055China

Growing studies have linked metal exposure to diabetes risk.However,these studies had inconsistent results.We used a multiple linear regression model to investigate the sexspecific and dose-response associations between urinary metals(cobalt(Co)and molybdenum(Mo))and diabetes-related indicators(fasting plasma glucose(FPG),hemoglobin A1c(HbA1c),homeostasis model assessment for Insulin resistance(HOMA-IR),and insulin)in a cross-sectional study based on the United States National Health and Nutrition Examination Survey.The urinary metal concentrations of 1423 eligible individuals were stratified on the basis of the quartile distribution.Our results showed that the urinary Co level in males at the fourth quartile(Q4)was strongly correlated with increased FPG(β=0.61,95%CI:0.17–1.04),HbA1c(β=0.31,95%CI:0.09–0.54),insulin(β=8.18,95%CI:2.84–13.52),and HOMA–IR(β=3.42,95%CI:1.40–5.44)when compared with first quartile(Q1).High urinary Mo levels(Q4 vs.Q1)were associated with elevated FPG(β=0.46,95%CI:0.17–0.75)and HbA1c(β=0.27,95%CI:0.11–0.42)in the overall population.Positive linear dose-response associations were observed between urinary Co and insulin(Pnonlinear=0.513)and HOMA–IR(Pnonlinear=0.736)in males,as well as a positive linear dose-response relationship between urinary Mo and FPG(Pnonlinear=0.826)and HbA1c(Pnonlinear=0.376)in the overall population.Significant sex-specific and dose-response relationships were observed between urinary metals(Co and Mo)and diabetes-related indicators,and the potential mechanisms should be further investigated.

关键词： Bayesian kernel machine regression Cobalt Diabetes Insulin resistance Molybdenum

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AstragalosideⅣameliorates insulin induced Insulin resistance in HepG2 cells through reactive oxygen species mediated c-Jun N-terminal kinase pathway

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Journal of Traditional Chinese Medicine 2023年第1期43卷 60-67页

作者： YE Xiaomei XING Xiaowei YUAN Kangrui WANG Dongming WU Dudu CHEN Zhi YU Zhiqiang School of Pharmacy Guangdong Medical UniversityDongguan 523808China Department of Clinical Pharmacy SSL Central Hospital of Dongguan City(the Third People's Hospital of Dongguan City)Dongguan 523326China Department of Pharmacy Central People's Hospital of ZhanjiangGuangzhou 510515China School of Pharmaceutical Sciences Guangdong Provincial Key Laboratory of New Drug ScreeningSouthern Medical UniversityZhanjiang 524037China

OBJECTIVE:To investigate the effects and elucidate the mechanism of Astragaloside IV(AS-IV)for Insulin resistance(IR)and type 2 diabet es mellitus(T2DM).METHODS:CCK8 kit was used to detect cell viability,glucose detection kit was used to detect the concentration of glucose in cell supernatant,reactive oxygen species(ROS)detection kit and Western blot were used to explore the mechanism of Astragaloside IV(AS-IV)in improving IR.A diabetic rat model was also established by feeding high sugar and fat diet and streptozotocin(STZ)injection.After treatment with AS-IV,rosiglitazone(ROZ),or normal saline,the fasting blood glucose(FBG),C peptide(C-P),tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and the glucose tolerance were assessed.RESULTS:AS-IV could effectively reduce the content of ROS and increase the glucose uptake in high insulintreated IR-type HepG 2 cells.The results of molecular mechanisms indicated that AS-IV could improve Insulin resistance by reducing JNK phosphorylation and regulating c-Jun N-terminal kinase(JNK)downstream protein expression.Additionally,AS-IV could significantly reduce the levels of FBG,TNF-α,IL-6 and the glucose tolerance in diabetic rats(PInsulin resistance of rats.

关键词： AstragalosideⅣ Insulin resistance Glucose consumption ROS JNK HepG2 cells

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Hereditary severe Insulin resistance syndrome:Pathogenesis,pathophysiology,and clinical management

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Genes & Diseases 2023年第5期10卷 1846-1856页

作者： Junaid Iqbal Hong-Li Jiang Hui-Xuan Wu Long Li Ying-Hui Zhou Nan Hu Fen Xiao Ting Wang Shi-Na Xu Hou-De Zhou National Clinical Research Center for Metabolic Diseases Hunan Provincial Key Laboratory for Metabolic Bone Diseasesand Department of Endocrinology and MetabolismThe Second XiangYa Hospital of Central South UniversityChangshaHunan 410011China

Severe Insulin resistance has been linked to some of the most globally prevalent disorders,such as diabetes mellitus,nonalcoholic fatty liver disease,polycystic ovarian syndrome,and hypertension.Hereditary severe Insulin resistance syndrome(H-SIRS)is a rare disorder classified into four principal categories:primary insulin receptor defects,lipodystrophies,complex syndromes,and obesity-related H-SIRS.Genes such as INSR,AKT2,TBC1D4,AGPAT2,BSCL2,CAV1,PTRF,LMNA,PPARG,PLIN1,CIDEC,LIPE,PCYT1A,MC4R,LEP,POMC,SH2B1,RECQL2,RECQL3,ALMS1,PCNT,ZMPSTE24,PIK3R1,and POLD1 have been linked to H-SIRS.Its clinical features include Insulin resistance,hyperglycemia,hyperandrogenism,severe dyslipidemia,fatty liver,abnormal topography of adipose tissue,and low serum leptin and adiponectin levels.Diagnosis of H-SIRS is based on the presence of typical clinical features associated with the various H-SIRS forms and the identification of mutations in H-SIRS-linked genes by genetic testing.Diet therapy,insulin sensitization,exogenous insulin therapy,and leptin replacement therapy have widely been adopted to manage H-SIRS.The rarity of H-SIRS,its highly variable clinical presentation,refusal to be tested for genetic mutations by patients’family members who are not severely sick,unavailability of genetic testing,and testing expenses contribute to the delayed or underdiagnoses of H-SIRS.Early diagnosis facilitates early management of the condition,which results in improved glycemic control and delayed onset of diabetes and other complications related to severe Insulin resistance.The use of updated genetic sequencing technologies is recommended,and long-term studies are required for genotype–phenotype differentiation and formulation of diagnostic and treatment protocols.

关键词： Diabetes Genetics Insulin resistance Lipodystrophy Pathophysiology Therapy

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Ocular manifestations of central Insulin resistance

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Neural Regeneration Research 2023年第5期18卷 1139-1146页

作者： Muneeb A.Faiq Trina Sengupta Madhu Nath Thirumurthy Velpandian Daman Saluja Rima Dada Tanuj Dada Kevin C.Chan Dr.Rajendra Prasad Centre for Ophthalmic Sciences All India Institute of Medical SciencesNew DelhiIndia Neuroimaging and Visual Science Laboratory Department of OphthalmologyNYU Grossman School of MedicineNYU Langone HealthNew York UniversityNew YorkNYUSA Medical Biotechnology Laboratory Dr.B.R.Ambedkar Center for Biomedical ResearchUniversity of DelhiDelhiIndia Dr.Baldev Singh Sleep Laboratory Department of PhysiologyAll India Institute of Medical SciencesNew DelhiIndia Department of Ocular Pharmacology Dr.Rajendra Prasad Center for Ophthalmic SciencesAll India Institute of Medical SciencesNew DelhiIndia Laboratory for Molecular Reproduction and Genetics Department of AnatomyAll India Institute of Medical SciencesNew DelhiIndia

Central Insulin resistance, the diminished cellular sensitivity to insulin in the brain, has been implicated in diabetes mellitus, Alzheimer’s disease and other neurological disorders. However, whether and how central Insulin resistance plays a role in the eye remains unclear. Here, we performed intracerebroventricular injection of S961, a potent and specific blocker of insulin receptor in adult Wistar rats to test if central Insulin resistance leads to pathological changes in ocular structures. 80 mg of S961 was stereotaxically injected into the lateral ventricle of the experimental group twice at 7 days apart, whereas buffer solution was injected to the sham control group. Blood samples, intraocular pressure, trabecular meshwork morphology, ciliary body markers, retinal and optic nerve integrity, and whole genome expression patterns were then evaluated. While neither blood glucose nor serum insulin level was significantly altered in the experimental or control group, we found that injection of S961 but not buffer solution significantly increased intraocular pressure at 14 and 24 days after first injection, along with reduced porosity and aquaporin 4 expression in the trabecular meshwork, and increased tumor necrosis factor α and aquaporin 4 expression in the ciliary body. In the retina, cell density and insulin receptor expression decreased in the retinal ganglion cell layer upon S961 injection. Fundus photography revealed peripapillary atrophy with vascular dysregulation in the experimental group. These retinal changes were accompanied by upregulation of pro-inflammatory and pro-apoptotic genes, downregulation of anti-inflammatory, anti-apoptotic, and neurotrophic genes, as well as dysregulation of genes involved in insulin signaling. Optic nerve histology indicated microglial activation and changes in the expression of glial fibrillary acidic protein, tumor necrosis factor α, and aquaporin 4. Molecular pathway architecture of the retina revealed the three most significant pathways involved being inflammation/

关键词： brain ciliary bodies gene expression inflammation insulin receptor Insulin resistance intraocular pressure neurodegeneration optic nerve retina retinal ganglion cells trabecular meshwork

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Lingguizhugan Decoction, a Chinese herbal formula, improves Insulin resistance in overweight/obese subjects with non-alcoholic fatty liver disease: a translational approach

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Frontiers of Medicine 2022年第5期16卷 745-759页

作者： Liang Dai Jingjuan Xu Baocheng Liu Yanqi Dang Ruirui Wang Lijie Zhuang Dong Li Lulu Jiao Jianying Wang Lei Zhang Linda LDZhong Wenjun Zhou Guang Ji Institute of Digestive Diseases Longhua HospitalShanghai University of Traditional Chinese MedicineShanghai 200032China Clinical Research Academy Peking University Shenzhen HospitalShenzhen 518032China Department of Integrated Traditional and Western Medicine Jinling HospitalMedical School of Nanjing UniversityNanjing 210002China Shanghai Innovation Centre of TCM Health Service Shanghai University of Traditional Chinese MedicineShanghai 201203China Sanlin Health Centre of Pudong New District Shanghai 200120China Zhangjiang Health Centre of Pudong New District Shanghai 201203China Beicai Health Centre of Pudong New District Shanghai 201204China Hong Kong Chinese Medicine Study Centre Hong Kong Baptist UniversityHong Kong 999077China

Lingguizhugan Decoction(LGZG)has been investigated in basic studies,with satisfactory effects on Insulin resistance in non-alcoholic fatty liver disease(NAFLD).This translational approach aimed to explore the effect and underlying mechanism of LGZG in clinical setting.A randomized,double-blinded,placebo-controlled trial was performed.A total of 243 eligible participants with NAFLD were equally allocated to receive LGZG(two groups:standard dose and low dose)or placebo for 12 weeks on the basis of lifestyle modifications.The primary efficacy variable was homeostasis model assessment of Insulin resistance(HOMA-IR).Analyses were performed in two populations in accordance with body mass index(BMI;overweight/obese,BMI 24 kg/m^(2);lean,BMIInsulin resistance in overweight/obese subjects with NAFLD.The underlying mechanism may be related to the regulation of DNA N6-methyladenine modification of PPP1R3A and ATG3.Lean subjects may not be a targeted population for LGZG.

关键词： Insulin resistance non-alcoholic fatty liver disease Chinese herbal medicine randomized controlled trial DNA N6-methyladenine modification

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Associations of Insulin resistance and beta-cell function with abnormal lipid profile in newly diagnosed diabetes

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Chinese Medical Journal 2022年第21期135卷 2554-2562页

作者： Xiaohan Tang Xiang Yan Houde Zhou Gan Huang Xiaohong Niu Hongwei Jiang Heng Su Xilin Yang Xia Li Zhiguang Zhou Department of Metabolism and Endocrinology National Clinical Research Center for Metabolic DiseasesKey Laboratory of Diabetes Immunology(Central South University)Ministry of EducationThe Second Xiangya Hospital of Central South UniversityChangshaHunan 410011China Department of Metabolism and Endocrinology National Clinical Research Center for Metabolic DiseasesHunan Provincial Key Laboratory for Metabolic Bone DiseasesThe Second Xiangya Hospital of Central South UniversityChangshaHunan 410011China Department of Endocrinology Heji Hospital Affiliated to Changzhi Medical CollegeChangzhiShanxi 046000China Department of Endocrinology The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and TechnologyLuoyangHenan 471003China Department of Endocrinology The Affiliated Hospital of Kunming University of Science and TechnologyThe First People’s Hospital of YunnanKunmingYunnan 650032China Department of Epidemiology and Biostatistics School of Public HealthTianjin Medical UniversityTianjin 300070China

Background:Abnormal lipids are strong predictors of cardiovascular disease in type 1 diabetes mellitus(T1DM)and type 2 diabetes mellitus(T2DM).However,the potential associations of Insulin resistance(IR)and beta-cell function(BCF)with abnormal lipids in newly diagnosed T1DM or T2DM patients are not fully understood.Methods:A cross-sectional survey of 15,928 participants was conducted.Homeostasis model assessment and postprandial C-peptide levels were used to estimate IR and BCF.A restricted cubic spline(RCS)nested in binary logistic regression was used to examine the associations of IR and BCF with abnormal lipids.Results:High triglyceride(TG),low high-density lipoprotein cholesterol,and high low-density lipoprotein cholesterol(LDL-C)accounted for 49.7%,47.8%,and 59.2%of the participants,respectively.In multivariable analysis,high IR was associated with an increased risk of high TGs(P for trend<0.001)in T1DM and is associated with an elevated risk of high TG and low HDL-C(all P for trend<0.01)in T2DM.Low BCF was not associated with risks of dyslipidemia in patients with T1DM or T2DM after adjustment for potential confounders.Conclusion:High IR had different associations with the risk of dyslipidemia in newly diagnosed T1DM and T2DM patients,suggesting that early treatment that improves IR may benefit abnormal lipid metabolism.

关键词： Beta-cell function Dyslipidemia Insulin resistance Type 1 diabetes Type 2 diabetes

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The mechanisms of nucleotide actions in Insulin resistance

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Journal of Genetics and Genomics 2022年第4期49卷 299-307页

作者： Kunpeng Liu Xiaogao Jin Xiaoying Zhang Hongkai Lian Jianping Ye Metabolic Disease Research Center Zhengzhou University Affiliated Zhengzhou Central HospitalZhengzhouHenan 450007China Cell-gene Therapy Translational Medicine Research Center The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Center for Advanced Medicine College of MedicineZhengzhou UniversityZhengzhouHenan 450007China Department of Orthopedics Zhengzhou Central HospitalZhengzhouHenan 450000China

Insulin resistance contributes to metabolic disorders in obesity and type 2 diabetes.In mechanisms of Insulin resistance,the roles of glucose,fatty acids,and amino acids have been extensively documented in literature.However,the activities of nucleotides remain to be reviewed comprehensively in the regulation of insulin sensitivity.Nucleotides are well known for their activities in biosynthesis of DNA and RNA as well as their signaling activities in the form of c AMP and c GAMP.Their activities in Insulin resistance are dependent on the derivatives and corresponding receptors.ATP and NADH,derivatives of adenosine,inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1,respectively.ATP,ADP and AMP,the well-known energy carriers,regulate cellular responses to insulin outside cells through the purinergic receptors in cell surface.Current evidence suggests that ATP,NADH,c GAMP,and uridine are potential biomarkers of Insulin resistance.However,GTP and c GMP are likely the markers of insulin sensitization.Here,studies crossing the biomedical fields are reviewed to characterize nucleotide activities in the regulation of insulin sensitivity.The knowledge brings new insights into the mechanisms of Insulin resistance.

关键词： Insulin resistance Nucleotide Adenosine Guanosine Uridine AMPK Purinergic receptors

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KAT7/HMGN1 signaling epigenetically induces tyrosine phosphorylation-regulated kinase 1A expression to ameliorate Insulin resistance in Alzheimer’s disease

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World Journal of Psychiatry 2024年第3期14卷 445-455页

作者： Qun-Shan Lu Lin Ma Wen-Jing Jiang Xing-Bang Wang Mei Lu Department of Geriatric Medicine Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina Key Laboratory of Cardiovascular Proteomics of Shandong Province Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina

BACKGROUND Epidemiological studies have revealed a correlation between Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2D).Insulin resistance in the brain is a common feature in patients with T2D and AD.KAT7 is a histone acetyltransferase that participates in the modulation of various genes.AIM To determine the effects of KAT7 on insulin patients with AD.METHODS APPswe/PS1-dE9 double-transgenic and db/db mice were used to mimic AD and diabetes,respectively.An in vitro model of AD was established by Aβstimulation.Insulin resistance was induced by chronic stimulation with high insulin levels.The expression of microtubule-associated protein 2(MAP2)was assessed using immunofluorescence.The protein levels of MAP2,Aβ,dual-specificity tyrosine phosphorylation-regulated kinase-1A(DYRK1A),IRS-1,p-AKT,total AKT,p-GSK3β,total GSK3β,DYRK1A,and KAT7 were measured via western blotting.Accumulation of reactive oxygen species(ROS),malondialdehyde(MDA),and SOD activity was measured to determine cellular oxidative stress.Flow cytometry and CCK-8 assay were performed to evaluate neuronal cell death and proliferation,respectively.Relative RNA levels of KAT7 and DYRK1A were examined using quantitative PCR.A chromatin immunoprecipitation assay was conducted to detect H3K14ac in DYRK1A.RESULTS KAT7 expression was suppressed in the AD mice.Overexpression of KAT7 decreased Aβaccumulation and MAP2 expression in AD brains.KAT7 overexpression decreased ROS and MDA levels,elevated SOD activity in brain tissues and neurons,and simultaneously suppressed neuronal apoptosis.KAT7 upregulated levels of p-AKT and p-GSK3βto alleviate Insulin resistance,along with elevated expression of DYRK1A.KAT7 depletion suppressed DYRK1A expression and impaired H3K14ac of DYRK1A.HMGN1 overexpression recovered DYRK1A levels and reversed Insulin resistance caused by KAT7 depletion.CONCLUSION We determined that KAT7 overexpression recovered insulin sensitivity in AD by recruiting HMGN1 to enhance DYRK1A acetylation.Our findings suggest that KAT7 is a novel and

关键词： Alzheimer's disease Diabetes Insulin resistance KAT7 Dual-specificity tyrosine phosphorylation-regulated kinase-1A HMGN1

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Ccrl2 deficiency deteriorates obesity and Insulin resistance through increasing adipose tissue macrophages infiltration

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Genes & Diseases 2022年第2期9卷 429-442页

作者： Min Xu Yu-Meng Wang Wan-Qing Li Cheng-Long Huang Jun Li Wen-Hua Xie Hong-Xiang Zeng Lin-Fen Tao Xi Li Biology Science Institutes Chongqing Medical UniversityChongqing 400016PR China

Obesity-induced inflammation,characterized by augmented infiltration and altered balance of macrophages,is a critical component of systemic Insulin resistance.Chemokine-chemokine receptor system plays a vital role in the macrophages accumulation.CC-Chemokine Receptor-like 2(Ccrl2)is one of the receptors of Chemerin,which is a member of atypical chemokine receptors(ACKR)family,reported taking part in host immune responses and inflammation-related conditions.In our study,we found ccrl2 expression significantly elevated in visceral adipose tissue(VAT)of high fat diet(HFD)induced obese mice and ob/ob mice.Systemic deletion of Ccrl2 gene aggravated HFD induced obesity and Insulin resistance and ccrl2−/−mice showed aggravated VAT inflammation and increased M1/M2 macrophages ratio,which is due to the increase of macrophages chemotaxis in Ccrl2 deficiency mice.Cumulatively,these results indicate that Ccrl2 has a critical function in obesity and obesity-induced Insulin resistance via mediating macrophages chemotaxis.

关键词： Ccrl2 Inflammation Insulin resistance Macrophages Obesity

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Double-edged effect of sodium citrate in Nile tilapia(Oreochromis niloticus):Promoting lipid and protein deposition vs.causing hyperglycemia and Insulin resistance

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Animal Nutrition 2023年第3期14卷 303-314页

作者： Jun-Xian Wang Fang Qiao Mei-Ling Zhang Li-Qiao Chen Zhen-Yu Du Yuan Luo Laboratory of Aquaculture Nutrition and Environmental Health(LANEH) School of Life SciencesEast China Normal UniversityShanghaiChina

Citrate is an essential substrate for energy metabolism that plays critical roles in regulating glucose and lipid metabolic homeostasis.However,the action of citrate in regulating nutrient metabolism in fish remains poorly understood.Here,we investigated the effects of dietary sodium citrate on growth performance and systematic energy metabolism in juvenile Nile tilapia(Oreochromis niloticus).A total of 270Nile tilapia(2.81±0.01 g)were randomly divided into three groups(3 replicates per group,30 fish per replicate)and fed with control diet(35%protein and 6%lipid),2%and 4%sodium citrate diets,respectively,for 8 weeks.The results showed that sodium citrate exhibited no effect on growth performance(P>0.05).The whole-body crude protein,serum triglyceride and hepatic glycogen contents were significantly increased in the 4%sodium citrate group(P0.05).The 4%sodium citrate treatment significantly increased the serum glucose and insulin levels at the end of feeding trial and also in the glucose tolerance test(P<0.05).The 4%sodium citrate significantly enhanced the hepatic phosphofructokinase activity and inhibited the expression of pyruvate dehydrogenase kinase isozyme 2 and phosphor-pyruvate dehydrogenase E1 component subunit alpha proteins(P<0.05).Additionally,the 4%sodium citrate significantly increased hepatic triglyceride and acetyl-Co A levels,while the expressions of carnitine palmitoyl transferase 1a protein were significantly down-regulated by the 4%sodium citrate(P<0.05).Besides,the 4%sodium citrate induced crude protein deposition in muscle by activating m TOR signaling and inhibiting AMPK signaling(P<0.05).Furthermore,the 4%sodium citrate significantly suppressed serum aspartate aminotransferase and alanine aminotransferase activities,along with the lowered expression of pro-inflammatory genes,such as nfκb,tnfa and il8(P<0.05).Although the 4%sodium citrate significantly increased phosphor-nuclear factor-k B p65 protein expression(P<0.05),no significant tissue dama

关键词： Sodium citrate Lipid and protein deposition Insulin resistance Nile tilapia

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