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hyperinsulinemia,Insulin Resistance and Cognitive Decline in Older Cohort

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Biomedical and Environmental Sciences 2012年第1期25卷 8-14页

作者： ZHONG Yuan MIAO Ya JIA Wei Ping YAN Hong WANG Bei Yun JIN Jun Department of Geriatrics Sixth People＇s Hospital Affiliated to Shanghai Jiao Tong University Shanghai 200233 China Department of Endocrinology and Metabolism Sixth People＇s Hospital Affiliated to Shanghai Jiao Tong University Shanghai Diabetes Institute Shanghai 200233 China

Objective decline of resistance whether H Type 2 diabetes has been recently recognized as an important risk factor for cognitive patients with Alzheimer＇s disease （AD）. But the roles of hyperinsulinemia （HI） and insulin （IR） in the development of AD are still controversial. This study was designed to evaluate or IR influenced the cognitive functions of older cohort. Methods The cognitive functions of 328 consecutive elderly patients were evaluated with a battery of cognitive rating scales. Their fasting blood glucose （FBG） and fasting insulin （FINS） were analyzed and IR was calculated with modified-Homa. The cognitive scores in different groups and the correlation of cognitive functions with HI or IR were analyzed. Results In our study, there were 180 participants with HI and 148 without HI, and 192 with iR and 136 without IR. The participants with HI showed worse cognitive functions than those without HI in MMSE, MOCA, CDR, orientation, delayed memory, and attention/calculation domains. Similarly, the elderly with IR had lower cognitive scores than those without IR in MMSE, MOCA, CDR, GDS, orientation, delayed memory, and attention/calculation domains. The insulin levels and Homa IR had negative correlation with the scores of MMSE and delayed memory, not only in the model I adjusted for FBG and diabetes history, but also in the model 2 adjusted for all nine demographic characteristics. Conclusion HI and IR are important risk factors for cognitive decline of the elderly, especially for the dysfunctions in delayed memory domains.

关键词： Cognitive function Alzheimer＇s disease hyperinsulinemia Insulin resistance

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BRSK2 in pancreatic β cells promotes hyperinsulinemia-coupled insulin resistance and its genetic variants are associated with human type 2 diabetes

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Journal of Molecular Cell Biology 2023年第5期15卷 21-37页

作者： Rufeng Xu Kaiyuan Wang Zhengjian Yao Yan Zhang Li Jin Jing Pang Yuncai Zhou Kai Wang Dechen Liu Yaqin Zhang Peng Sun Fuqiang Wang Xiaoai Chang Tengli Liu Shusen Wang Yalin Zhang Shuyong Lin Cheng Hu Yunxia Zhu Xiao Han Key Laboratory of Human Functional Genomics of Jiangsu Province Nanjing Medical UniversityNanjing 211166China Institute for Metabolic Disease Fengxian Central Hospital Affiliated to Southern Medical UniversityShanghai 201499China Shanghai Diabetes Institute Shanghai Key Laboratory of Diabetes MellitusShanghai Clinical Center for DiabetesShanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200233China Analysis Center Nanjing Medical UniversityNanjing 210029China Organ Transplant Center Tianjin First Central HospitalNankai UniversityTianjin 300192China State Key Laboratory for Cellular Stress Biology School of Life SciencesXiamen UniversityXiamen 361102China

Brain-specific serine/threonine-protein kinase 2(BRSK2)plays critical roles in insulin secretion andβ-cell biology.However,whether BRSK2 is associated with human type 2 diabetes mellitus(T2DM)has not been determined.Here,we report that BRSK2 genetic variants are closely related to worsening glucose metabolism due to hyperinsulinemia and insulin resistance in the Chinese population.BRSK2 protein levels are significantly elevated inβcells from T2DM patients and high-fat diet(HFD)-fed mice due to enhanced protein stability.Mice with inducibleβ-cell-specific Brsk2 knockout(βKO)exhibit normal metabolism with a high potential for insulin secretion under chow-diet conditions.Moreover,βKO mice are protected from HFD-induced hyperinsulinemia,obesity,insulin resistance,and glucose intolerance.Conversely,gain-of-function BRSK2 in matureβcells reversibly triggers hyperglycemia due toβ-cell hypersecretion-coupled insulin resistance.Mechanistically,BRSK2 senses lipid signals and induces basal insulin secretion in a kinase-dependent manner.The enhanced basal insulin secretion drives insulin resistance andβ-cell exhaustion and thus the onset of T2DM in mice fed an HFD or with gain-of-function BRSK2 inβcells.These findings reveal that BRSK2 links hyperinsulinemia to systematic insulin resistance via interplay betweenβcells and insulin-sensitive tissues in the populations carrying human genetic variants or under nutrient-overload conditions.

关键词： type 2 diabetes mellitus genetic variant BRSK2 β-cell hypersecretion hyperinsulinemia insulin resistance

hyperinsulinemia,cancer and maqui berry:The promise of nutritional supplementation

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Food Science and Human Wellness 2019年第3期8卷 264-267页

作者： Brett Deters Mir Saleem Halmos College of Natural Sciences and Oceanography NOVA Southeastern UniversityFort LauderdaleFL 33314USA

Nutritional supplementation has long been studied as a possible treatment alternative or as an adjunct to the standard treatments for common ailments and diseases.According to the latest research,the Chilean maqui berry,Aristotelia chilensis,has been shown to reduce postprandial insulin levels by as much as fifty percent.The berry,which has been shown to be as effective as metformin at increasing insulin sensitivity and controlling blood glucose levels,follows a simple mechanism of action that involves the inhibition of sodium dependent glucose transporters in the small intestine,slowing the rate at which sugars enter the bloodstream and thereby decreasing blood sugar spikes and the corresponding increase in insulin levels.Chronically high blood glucose levels have been proven to play a significant role in the development of cancers,as diabetics and prediabetics have been proven to have elevated risk of developing cancerous growth.Consistent dietary supplementation with maqui berry may therefore indirectly reduce the risk of cancer,as well as other diseases which respond negatively to hyperglycemia and hyperinsulinemia.

关键词： hyperinsulinemia Cardiovascular disease Diabetes Insulin Maqui berry Cancer

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Protein causes hyperinsulinemia： a Chinese patient with hyperinsulinism/hyperammonaemia syndrome due to a glutamate dehydrogenase gene mutation

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Chinese Medical Journal 2010年第13期123卷 1793-1795页

作者： CHEN Shi XIAO Xin-hua DIAO Cheng-ming TONG An-li WANG Ou QIU Zheng-qing YU Kang WANG Tong Department of Endocrinology eking Union Medical College Hospital Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 100730 China Department of Pediatrics Peking Union Medical College Hospital Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 100730 China Nutritional Department Peking Union Medical College Hospital Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 100730 China

Glucose is derived from three sources： intestinal absorption, glycogenolysis, and gluconeogenesis.Hypoglycemia in child is often attributed to depletion of glycogen stores. However, recently, congenital hyperinsulini... 详细信息

关键词： hyperinsulinisrn/hyperammonaemia syndrome hyperinsulinemia hypoglycemia

Adult focalβ-cell nesidioblastosis:A case report

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World Journal of Clinical Cases 2023年第1期11卷 150-156页

作者： Kui Tu Li-Jin Zhao Jin Gu Department of General Surgery Affiliated Hospital of Zunyi Medical UniversityZunyi 563000Guizhou ProvinceChina

BACKGROUND Nesidioblastosis usually refers to a series of clinical manifestations caused by the proliferation ofβ-cells in pancreatic islets,and these clinical manifestations are hyperinsulinemia and persistent hypoglycemia.According to the size of the lesion,nesidioblastosis is divided into focal nesidioblastosis,diffuse nesidioblastosis and atypical nesidioblastosis,and its pathogenesis is still unclear.Nesidioblastosis is mainly seen in infants and rarely reported in adults,especially focal nesidioblastosis,which is difficult to distinguish from insulinoma.CASE SUMMARY We report a case of adult focalβ-cell nesidioblastosis in which the preoperative diagnosis was insulinoma.The patient was a 48-year-old male who suffered from repeated morning and fasting palpitations,sweating,and severe disturbance of consciousness for 5 years.His blood glucose was found to be as low as 1.79 mmol/L during an attack.However,abdominal computed tomography showed no abnormalities.Magnetic resonance imaging and endoscopic ultrasonography demonstrated a nodular mass in the head of the pancreas,combined with hyperinsulinemia and high serum C-peptide.The patient was diagnosed with insulinoma and underwent Beger surgery;however,the postoperative pathological results showed nesidioblastosis.CONCLUSION Although surgical resection is the preferred option for nesidioblastosis,some cases can be treated non-surgically.In order to increase clinicians’understanding of nesidioblastosis,it is necessary to review the pathogenesis,diagnosis and treatment of this disease.

关键词： Focal nesidioblastosis hyperinsulinemia Persistent hypoglycemia Case report

Cognitive deficits and Alzheimer-like neuropathological impairments during adolescence in a rat model of type 2 diabetes mellitus

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Neural Regeneration Research 2018年第11期13卷 1995-2004页

作者： Li Jin Yi-Pei Li Qiong Feng Li Ren Fang Wang Guo-Jia Bo Li Wang Department of Pathophysiology Henan Medical College Henan Key Laboratory of Degenerative Brain Disease Henan Medical College Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and Technology Department of Pathology Wuhan Children's Hospital

Numerous studies have shown that many patients who suffer from type 2 diabetes mellitus exhibit cognitive dysfunction and neuronal synaptic impairments. Therefore, growing evidence suggests that type 2 diabetes mellitus has a close relationship with occurrence and progression of neurodegeneration and neural impairment in Alzheimer＇s disease. However, the relationship between metabolic disorders caused by type 2 diabetes mellitus and neurodegeneration and neural impairments in Alzheimer＇s disease is still not fully determined. Thus, in this study, we replicated a type 2 diabetic animal model by subcutaneous injection of newborn Sprague-Dawley rats with monosodium glutamate during the neonatal period. At 3 months old, the Barnes maze assay was performed to evaluate spatial memory function. Microelectrodes were used to measure electrophysiological function in the hippocampal CA1 region. Western blot assay was used to determine expression levels of glutamate ionotropic receptor NMDA type subunit 2 A（GluN2A） and GluN2B in the hippocampus. Enzyme-linked immunosorbent assay was used to determine levels of interleukin-1β, tumor necrosis factor α, and interleukin-6 in the hippocampus and cerebral cortex, as well as hippocampal amyloid beta（Aβ）1-40 and Aβ_（1-42） levels. Our results showed that in the rat model of type 2 diabetes mellitus caused by monosodium glutamate exposure during the neonatal period, latency was prolonged and the number of errors increased in the Barnes maze. Further, latency was increased and time in the escape platform quadrant shortened. Number of times crossing the platform was also reduced in the Morris water maze. After high frequency stimulation of the hippocampus, synaptic transmission was inhibited, expression of GluN2A and GluN2B were decreased in the hippocampus, expression of interleukin 1β, interleukin 6, and tumor necrosis factor α was increased in the hippocampus and cortex, and levels of Aβ_（1-40） and Aβ_（1-42） were increased in the hippocampus. These findings confirm that type 2 diabet

关键词： nerve regeneration type 2 diabetes mellitus Alzheimer＇s disease monosodium glutamate neonatal period cognitive deficits hyperglycemia hyperinsulinemia insulin resistance neural regeneration

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Mechanism of insulin resistance in obesity: a role of ATP

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Frontiers of Medicine 2021年第3期15卷 372-382页

作者： Jianping Ye Shanghai Diabetes Institute Shanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghai 200233China

Obesity increases the risk of type 2 diabetes through the induction of insulin resistance.The mechanism of insulin resistance has been extensively investigated for more than 60 years,but the essential pathogenic signal remains missing.Existing hypotheses include inflammation,mitochondrial dysfunction,hyperinsulinemia,hyperglucagonemia,glucotoxicity,and lipotoxicity.Drug discoveries based on these hypotheses are unsuccessful in the development of new medicines.In this review,multidisciplinary literature is integrated to evaluate ATP as a primary signal for insulin resistance.The ATP production is elevated in insulin-sensitive cells under obese conditions independent of energy demand,which we have named“mitochondrial overheating.”Overheating occurs because of substrate oversupply to mitochondria,leading to extra ATP production.The ATP overproduction contributes to the systemic insulin resistance through several mechanisms,such as inhibition of AMPK,induction of mTOR,hyperinsulinemia,hyperglucagonemia,and mitochondrial dysfunction.Insulin resistance represents a feedback regulation of energy oversupply in cells to control mitochondrial overloading by substrates.Insulin resistance cuts down the substrate uptake to attenuate mitochondrial overloading.The downregulation of the mitochondrial overloading by medicines,bypass surgeries,calorie restriction,and physical exercise leads to insulin sensitization in patients.Therefore,ATP may represent the primary signal of insulin resistance in the cellular protective response to the substrate oversupply.The prevention of ATP overproduction represents a key strategy for insulin sensitization.

关键词： type 2 diabetes energy expenditure mitochondria hyperinsulinemia hyperglucagonemia AMPK

Mechanisms of insulin resistance in obesity

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Frontiers of Medicine 2013年第1期7卷 14-24页

作者： Jianping Ye Antioxidant and Gene Regulation Laboratory Pennington Biomedical Research CenterLouisiana State University SystemBaton RougeLA70808USA

Obesity increases the risk for type 2 diabetes through induction of insulin resistance.Treatment of type 2 diabetes has been limited by little translational knowledge of insulin resistance although there have been several well-documented hypotheses for insulin resistance.In those hypotheses,inflammation,mitochondrial dysfunction,hyperinsulinemia and lipotoxicity have been the major concepts and have received a lot of attention.Oxidative stress,endoplasmic reticulum(ER)stress,genetic background,aging,fatty liver,hypoxia and lipodystrophy are active subjects in the study of these concepts.However,none of those concepts or views has led to an effective therapy for type 2 diabetes.The reason is that there has been no consensus for a unifying mechanism of insulin resistance.In this review article,literature is critically analyzed and reinterpreted for a new energy-based concept of insulin resistance,in which insulin resistance is a result of energy surplus in cells.The energy surplus signal is mediated by ATP and sensed by adenosine monophosphate-activated protein kinase(AMPK)signaling pathway.Decreasing ATP level by suppression of production or stimulation of utilization is a promising approach in the treatment of insulin resistance.In support,many of existing insulin sensitizing medicines inhibit ATP production in mitochondria.The effective therapies such as weight loss,exercise,and caloric restriction all reduce ATP in insulin sensitive cells.This new concept provides a unifying cellular and molecular mechanism of insulin resistance in obesity,which may apply to insulin resistance in aging and lipodystrophy.

关键词： type 2 diabetes energy expenditure inflammation lipotoxicity mitochondria hyperinsulinemia adenosine monophosphate-activated protein kinase(AMPK)

Therapeutic effects of tender coconut water on oxidative stress in fructose fed insulin resistant hypertensive rats

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Asian Pacific Journal of Tropical Medicine 2012年第4期5卷 270-276页

作者： D Bhagya L Prema T Rajamohan Department of Biochemistry University of Kerala.Kariavattom CampusKeralaTrivandrum695581India Department of Food Science and Nutrition Agricultural CollegeVellayaniTrivandrumKeralaIndia Department of Biochemistry University of Kerala Kariavattom CampusKeralaTrivandrum695581India

Objective:To investigate whether tender coconut water(TCW) mitigates oxidative stress in fructose fed hypertensive rats.Methods:Male Sprague Dawley rats were fed with fructose rich diet and treated with TCW(4 mL/100 g of body weight) for 3 subsequent weeks.Systolic blootl pressure was measured every three days using the indirect tail cuff method.At the end of the experimental period,plasma glucose and insulin,serum triglycerides and free fatly acids, lipid peroxidation markers(MDA,hydroperoxides and conjugated dienes) and the activities of antioxidant enzymes were analyzed in all the groups.Results:Treatment with TCW significandy lowered the systolic blood pressure and reduced serum triglycerides and free fatty acids.Plasma glucose and insulin levels and lipid peroxidation markers such as MDA,hydroperoxides and conjugated dienes were significantly reduced in fructose fed rats treated with TCW.Activities of antioxidant enzymes are up regulated significantly in TCW treated rats.Hislopathological analysis of liver showed that TCW treatment reduced the lipid accumulation and inflammatory infiltration without any significant hepatocellular damage.Conclusions:The overall results suggest that, TCW treatment could prevent and reverse high blood pressure induced by high fructose diet probably by inhibition of lipid peroxidation,upregulation of antioxidant status and improved insulin sensitivity.

关键词： Tender coconut water Hypertension Oxidative stress hyperinsulinemia Lipid peroxidation Histopathology