Perioperative insulin therapy

AbstractSurgical patients commonly develop hyperglycemia secondary to the neuroendocrine stress response. Insulin treatment of hyperglycemia is required to overcome the perioperative catabolic state and acute insulin resistance. Besides its metabolic actions on glucose metabolism, insulin also displays nonmetabolic physiological effects. Preoperative glycemic assessment, maintenance of normoglycemia, and avoidance of glucose variability are paramount to optimize surgical outcomes. This review discusses the basic physiology and effects of insulin as well as practical issues pertaining to its management during the perioperative period.

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Application of exercised-based pre-rehabilitation in perioperative period of patients with gastric cancer

Open Medicine ◽

10.1515/med-2019-0103 ◽

2019 ◽

Vol 14 (1) ◽

pp. 875-882

Author(s):

Wu Jianjun ◽

Wu Xing ◽

Yao Guozhong ◽

Zhu Chuming ◽

Yan Jiang

Keyword(s):

Gastric Cancer ◽

Insulin Resistance ◽

Stress Response ◽

Treatment Group ◽

Inflammatory Response ◽

Nutritional Status ◽

Perioperative Period ◽

Postoperative Recovery ◽

Postoperative Rehabilitation ◽

Gastric Cancer Patients

AbstractObjectiveTo analyze the difference between exercised-based pre-rehabilitation and postoperative rapid rehabilitation of gastric cancer patients.MethodsThe clinical data of 120 patients who underwent surgical treatment between 2016 and 2018 in our hospital with pathologically confirmed gastric cancer were retrospectively reviewed. According to the different treatments during the perioperative period, they were divided into exercised-based pre-rehabilitation group and postoperative rapid rehabilitation group. Factor analysis was used to analyze pre-rehabilitation and postoperative rehabilitation of patients with gastric cancer after stress response, nutritional status, insulin resistance, and inflammatory response in patients with gastric cancer, and to further evaluate the value of pre-recovery accelerated postoperative recovery.ResultsThe postoperative stress response, insulin resistance, and inflammatory response in the pre-rehabilitation group were lower than the conventional treatment group. The nutritional status was improved faster than the traditional treatment group. Exercised-based pre-rehabilitation for the rapid recovery of postoperative gastrointestinal function in patients with gastric cancer surgery has significant value.ConclusionExercised-based pre-rehabilitation has great significance for the accelerated rehabilitation of patients with gastric cancer during perioperative period.

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The Effect of FGF-21 on Glucose Metabolism in The Resistin-induced Insulin Resistance Liver Cells

ACTA AGRONOMICA SINICA ◽

10.3724/sp.j.1206.2012.00462 ◽

2013 ◽

Vol 40 (6) ◽

pp. 524

Author(s):

Miao LIU ◽

Wen-Fei WANG ◽

Ming-Yao LIU ◽

Jing-Zhuang ZHAO ◽

Yin BAI ◽

...

Keyword(s):

Insulin Resistance ◽

Glucose Metabolism ◽

Liver Cells

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Brain Glucose Metabolism in Health, Obesity, and Cognitive Decline—Does Insulin Have Anything to Do with It? A Narrative Review

Journal of Clinical Medicine ◽

10.3390/jcm10071532 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1532

Author(s):

Eleni Rebelos ◽

Juha O. Rinne ◽

Pirjo Nuutila ◽

Laura L. Ekblad

Keyword(s):

Insulin Resistance ◽

Glucose Metabolism ◽

Cognitive Decline ◽

Fdg Pet ◽

Metabolic Disorders ◽

Brain Glucose ◽

Brain Glucose Metabolism ◽

Systemic Insulin Resistance ◽

Increased Risk ◽

18F Fdg

Imaging brain glucose metabolism with fluorine-labelled fluorodeoxyglucose ([18F]-FDG) positron emission tomography (PET) has long been utilized to aid the diagnosis of memory disorders, in particular in differentiating Alzheimer’s disease (AD) from other neurological conditions causing cognitive decline. The interest for studying brain glucose metabolism in the context of metabolic disorders has arisen more recently. Obesity and type 2 diabetes—two diseases characterized by systemic insulin resistance—are associated with an increased risk for AD. Along with the well-defined patterns of fasting [18F]-FDG-PET changes that occur in AD, recent evidence has shown alterations in fasting and insulin-stimulated brain glucose metabolism also in obesity and systemic insulin resistance. Thus, it is important to clarify whether changes in brain glucose metabolism are just an epiphenomenon of the pathophysiology of the metabolic and neurologic disorders, or a crucial determinant of their pathophysiologic cascade. In this review, we discuss the current knowledge regarding alterations in brain glucose metabolism, studied with [18F]-FDG-PET from metabolic disorders to AD, with a special focus on how manipulation of insulin levels affects brain glucose metabolism in health and in systemic insulin resistance. A better understanding of alterations in brain glucose metabolism in health, obesity, and neurodegeneration, and the relationships between insulin resistance and central nervous system glucose metabolism may be an important step for the battle against metabolic and cognitive disorders.

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Impact of Glucose Metabolism Disorders on IGF-1 Levels in Patients with Acromegaly

Hormone and Metabolic Research ◽

10.1055/a-0594-2404 ◽

2018 ◽

Vol 50 (05) ◽

pp. 408-413 ◽

Cited By ~ 1

Author(s):

Sema Dogansen ◽

Gulsah Yalin ◽

Seher Tanrikulu ◽

Sema Yarman

Keyword(s):

Diabetes Mellitus ◽

Insulin Resistance ◽

Glucose Metabolism ◽

Glucose Tolerance ◽

Normal Glucose Tolerance ◽

Glucose Metabolism Disorders ◽

Insulin Resistant ◽

Normal Glucose ◽

Resistant Group ◽

The Impact

AbstractIn this study, we aimed to evaluate the presence of glucose metabolism abnormalities and their impact on IGF-1 levels in patients with acromegaly. Ninety-three patients with acromegaly (n=93; 52 males/41 females) were included in this study. Patients were separated into three groups such as; normal glucose tolerance (n=23, 25%), prediabetes (n=38, 41%), and diabetes mellitus (n=32, 34%). Insulin resistance was calculated with homeostasis model assessment (HOMA). HOMA-IR > 2.5 or ≤2.5 were defined as insulin resistant or noninsulin resistant groups, respectively. Groups were compared in terms of factors that may be associated with glucose metabolism abnormalities. IGF-1% ULN (upper limit of normal)/GH ratios were used to evaluate the impact of glucose metabolism abnormalities on IGF-1 levels. Patients with diabetes mellitus were significantly older with an increased frequency of hypertension (p<0.001, p=0.01, respectively). IGF-1% ULN/GH ratio was significantly lower in prediabetes group than in normal glucose tolerance group (p=0.04). Similarly IGF-1% ULN/GH ratio was significantly lower in insulin resistant group than in noninsulin resistant group (p=0.04). Baseline and suppressed GH levels were significantly higher in insulin resistant group than in noninsulin resistant group (p=0.024, p<0.001, respectively). IGF-1% ULN/GH ratio is a useful marker indicating glucose metabolism disorders and IGF-1 levels might be inappropriately lower in acromegalic patients with insulin resistance or prediabetes. We suggest that IGF-1 levels should be re-evaluated after the improvement of insulin resistance or glycemic regulation for the successful management of patients with acromegaly.

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Beneficial Effect of Pistachio Consumption on Glucose Metabolism, Insulin Resistance, Inflammation, and Related Metabolic Risk Markers: A Randomized Clinical Trial

Diabetes Care ◽

10.2337/dc14-1431 ◽

2014 ◽

Vol 37 (11) ◽

pp. 3098-3105 ◽

Cited By ~ 56

Author(s):

Pablo Hernández-Alonso ◽

Jordi Salas-Salvadó ◽

Mònica Baldrich-Mora ◽

Martí Juanola-Falgarona ◽

Mònica Bulló

Keyword(s):

Insulin Resistance ◽

Clinical Trial ◽

Glucose Metabolism ◽

Beneficial Effect ◽

Randomized Clinical Trial ◽

Metabolic Risk ◽

Risk Markers

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Serine Phosphorylation Proximal to Its Phosphotyrosine Binding Domain Inhibits Insulin Receptor Substrate 1 Function and Promotes Insulin Resistance

Molecular and Cellular Biology ◽

10.1128/mcb.24.21.9668-9681.2004 ◽

2004 ◽

Vol 24 (21) ◽

pp. 9668-9681 ◽

Cited By ~ 83

Author(s):

Yan-Fang Liu ◽

Avia Herschkovitz ◽

Sigalit Boura-Halfon ◽

Denise Ronen ◽

Keren Paz ◽

...

Keyword(s):

Insulin Resistance ◽

Insulin Receptor ◽

Insulin Signaling ◽

Insulin Treatment ◽

Binding Domain ◽

Serine Phosphorylation ◽

Insulin Receptor Substrate ◽

Control Mechanisms ◽

Insulin Receptor Substrate 1 ◽

Phosphotyrosine Binding Domain

ABSTRACT Ser/Thr phosphorylation of insulin receptor substrate (IRS) proteins negatively modulates insulin signaling. Therefore, the identification of serine sites whose phosphorylation inhibit IRS protein functions is of physiological importance. Here we mutated seven Ser sites located proximal to the phosphotyrosine binding domain of insulin receptor substrate 1 (IRS-1) (S265, S302, S325, S336, S358, S407, and S408) into Ala. When overexpressed in rat hepatoma Fao or CHO cells, the mutated IRS-1 protein in which the seven Ser sites were mutated to Ala (IRS-17A), unlike wild-type IRS-1 (IRS-1WT), maintained its Tyr-phosphorylated active conformation after prolonged insulin treatment or when the cells were challenged with inducers of insulin resistance prior to acute insulin treatment. This was due to the ability of IRS-17A to remain complexed with the insulin receptor (IR), unlike IRS-1WT, which underwent Ser phosphorylation, resulting in its dissociation from IR. Studies of truncated forms of IRS-1 revealed that the region between amino acids 365 to 430 is a main insulin-stimulated Ser phosphorylation domain. Indeed, IRS-1 mutated only at S408, which undergoes phosphorylation in vivo, partially maintained the properties of IRS-17A and conferred protection against selected inducers of insulin resistance. These findings suggest that S408 and additional Ser sites among the seven mutated Ser sites are targets for IRS-1 kinases that play a key negative regulatory role in IRS-1 function and insulin action. These sites presumably serve as points of convergence, where physiological feedback control mechanisms, which are triggered by insulin-stimulated IRS kinases, overlap with IRS kinases triggered by inducers of insulin resistance to terminate insulin signaling.

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12/15-Lipoxygenase signaling in the endoplasmic reticulum stress response

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00373.2011 ◽

2012 ◽

Vol 302 (6) ◽

pp. E654-E665 ◽

Cited By ~ 35

Author(s):

Banumathi K. Cole ◽

Norine S. Kuhn ◽

Shamina M. Green-Mitchell ◽

Kendall A. Leone ◽

Rebekah M. Raab ◽

...

Keyword(s):

Insulin Resistance ◽

Endoplasmic Reticulum ◽

Stress Response ◽

Er Stress ◽

Pancreatic Islets ◽

High Fat Diet ◽

Wild Type ◽

High Fat ◽

Stress Markers ◽

Deficient Mice

Central obesity is associated with chronic inflammation, insulin resistance, β-cell dysfunction, and endoplasmic reticulum (ER) stress. The 12/15-lipoxygenase enzyme (12/15-LO) promotes inflammation and insulin resistance in adipose and peripheral tissues. Given that obesity is associated with ER stress and 12/15-LO is expressed in adipose tissue, we determined whether 12/15-LO could mediate ER stress signals. Addition of 12/15-LO lipid products 12(S)-HETE and 12(S)-HPETE to differentiated 3T3-L1 adipocytes induced expression and activation of ER stress markers, including BiP, XBP-1, p-PERK, and p-IRE1α. The ER stress inducer, tunicamycin, upregulated ER stress markers in adipocytes with concomitant 12/15-LO activation. Addition of a 12/15-LO inhibitor, CDC, to tunicamycin-treated adipocytes attenuated the ER stress response. Furthermore, 12/15-LO-deficient adipocytes exhibited significantly decreased tunicamycin-induced ER stress. 12/15-LO action involves upregulation of interleukin-12 (IL-12) expression. Tunicamycin significantly upregulated IL-12p40 expression in adipocytes, and IL-12 addition increased ER stress gene expression; conversely, LSF, an IL-12 signaling inhibitor, and an IL-12p40-neutralizing antibody attenuated tunicamycin-induced ER stress. Isolated adipocytes and liver from 12/15-LO-deficient mice fed a high-fat diet revealed a decrease in spliced XBP-1 expression compared with wild-type C57BL/6 mice on a high-fat diet. Furthermore, pancreatic islets from 12/15-LO-deficient mice showed reduced high-fat diet-induced ER stress genes compared with wild-type mice. These data suggest that 12/15-LO activity participates in ER stress in adipocytes, pancreatic islets, and liver. Therefore, reduction of 12/15-LO activity or expression could provide a new therapeutic target to reduce ER stress and downstream inflammation linked to obesity.

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Stress and Its Effects on Glucose Metabolism and 11-HSD Activities in Rats Fed on a Combination of High-Fat and High-Sucrose Diet with Glycyrrhizic Acid

Journal of Diabetes Research ◽

10.1155/2013/190395 ◽

2013 ◽

Vol 2013 ◽

pp. 1-18 ◽

Cited By ~ 7

Author(s):

Hamish Alexander Fernando ◽

Hsien-Fei Chin ◽

So Ha Ton ◽

Khalid Abdul Kadir

Keyword(s):

Stress Response ◽

Glucose Metabolism ◽

Glycyrrhizic Acid ◽

Moderate Intensity ◽

Sucrose Diet ◽

Unhealthy Diet ◽

High Sucrose Diet ◽

Subcutaneous Adipose ◽

High Sucrose ◽

Intensity Stress

Chronic stress has been shown to have a strong link towards metabolic syndrome (MetS). Glycyrrhizic acid (GA) meanwhile has been shown to improve MetS symptoms caused by an unhealthy diet by inhibiting 11β-HSD 1. This experiment aimed to determine the effects of continuous, moderate-intensity stress on rats with and without GA intake on systolic blood pressure (SBP) across a 28-day period, as well as glucose metabolism, and 11β-HSD 1 and 2 activities at the end of the 28-day period. Adaptation to the stressor (as shown by SBP) resulted in no significant defects in glucose metabolism by the end of the experimental duration. However, a weakly significant increase in renal 11β-HSD 1 and a significant increase in subcutaneous adipose tissue 11β-HSD 1 activities were observed. GA intake did not elicit any significant benefit in glucose metabolism, indicating that the stress response may block its effects. However, GA-induced improvements in 11β-HSD activities in certain tissues were observed, although it is uncertain if these effects are manifested after adaptation due to the withdrawal of the stress response. Hence the ability of GA to improve stress-induced disturbances in the absence of adaptation needs to be investigated further.

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Impact of disease activity on impaired glucose metabolism in patients with rheumatoid arthritis

Arthritis Research & Therapy ◽

10.1186/s13075-021-02476-0 ◽

2021 ◽

Vol 23 (1) ◽

Author(s):

Gorica G. Ristić ◽

Vesna Subota ◽

Dejana Stanisavljević ◽

Danilo Vojvodić ◽

Arsen D. Ristić ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Risk Factors ◽

Insulin Resistance ◽

Glucose Metabolism ◽

Disease Activity ◽

Impaired Glucose Metabolism ◽

Inflammation Markers ◽

C Peptide ◽

Related Risk ◽

The Impact

Abstract Objective To explore glucose metabolism in rheumatoid arthritis (RA) and its association with insulin resistance (IR) risk factors and disease activity indicators, including matrix metalloproteinase-3 (MMP3). Methods This single-center study included 127 non-diabetic subjects: 90 RA patients and 37 matched controls. IR-related risk factors, disease activity (DAS28-ESR/CRP), concentrations of inflammation markers, MMP3, glucose, specific insulin, and C-peptide (a marker of β-cell secretion) were determined. Homeostasis Model Assessment was used to establish insulin resistance (HOMA2-IR) and sensitivity (HOMA2-%S). Associations of HOMA2 indices with IR-related risk factors, inflammation markers, and RA activity were tested using multiple regression analyses. Results RA patients had significantly increased HOMA2-IR index than controls. In the RA group, multivariate analysis revealed DAS28-ESR, DAS28-CRP, tender joint counts, patient’s global assessment, and MMP3 level as significant positive predictors for HOMA2-IR (β = 0.206, P = 0.014; β = 0.192, P = 0.009; β = 0.121, P = 0.005; β = 0.148, P = 0.007; β = 0.075, P = 0.025, respectively), and reciprocal negative for HOMA2-%S index. According to the value of the coefficient of determination (R2), DAS28-ESR ≥ 5.1 has the largest proportion of variation in both HOMA2-IR indices. DAS28-ESR ≥ 5.1 and ESR were independent predictors for increased C-peptide concentration (β = 0.090, P = 0.022; β = 0.133, P = 0.022). Despite comparability regarding all IR-related risk factors, patients with DAS28-ESR ≥ 5.1 had higher HOMA2-IR than controls [1.7 (1.2–2.5) vs. 1.2 (0.8–1.4), P = 0.000]. There was no difference between patients with DAS28-ESR < 5.1 and controls [1.3 (0.9–1.9) vs. 1.2 (0.8–1.4), P = 0.375]. Conclusions RA activity is an independent risk factor for impaired glucose metabolism. DAS28-ESR ≥ 5.1 was the main contributor to this metabolic disturbance, followed by MMP3 concentration, outweighing the impact of classic IR-related risk factors.

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