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InsulinInsulin ResistanceRats, ZuckerObesityReceptor, InsulinGlucose Tolerance TestGlucose Clamp TechniqueBlood GlucoseGlucoseAdipose TissueSensitivity and SpecificityHypoglycemic AgentsBody WeightDiabetes Mellitus, Type 2HyperinsulinismMuscle, SkeletalInsulin Receptor Substrate ProteinsFastingThinnessLiverGlucose IntoleranceTriglyceridesFatty Acids, NonesterifiedLeptinEatingAdiponectinThiazolidinedionesDiet, High-FatInsulin-Secreting CellsBody CompositionAdipocytesLipid MetabolismDietary FatsRats, Mutant StrainsIslets of LangerhansLipidsC-PeptideGlucose Transporter Type 4HyperglycemiaAdiposityHomeostasisEnergy MetabolismMetforminRats, WistarInsulin, Long-ActingSodium GlutamateDietBody Mass IndexSignal TransductionInsulin AntagonistsReference ValuesMice, ObeseMetabolic Syndrome XInsulin AntibodiesDiabetes Mellitus, ExperimentalPrediabetic StateAnti-Obesity AgentsGlucagonFatty AcidsTime FactorsLipolysisRats, Sprague-DawleyGlycogenDiabetes Mellitus3T3-L1 CellsPPAR gammaDietary CarbohydratesDisease Models, AnimalWeight LossIntra-Abdominal FatThiazolesPhosphorylationFatty LiverRNA, MessengerMonosaccharide Transport ProteinsBlood PressureEnergy IntakeInsulin Infusion SystemsDose-Response Relationship, DrugInsulin LisproMice, Inbred C57BLGlucagon-Like Peptide 1Organ SizeCaloric RestrictionWeight GainProinsulinPostprandial PeriodMice, KnockoutPolycystic Ovary SyndromePhysical Conditioning, AnimalProto-Oncogene Proteins c-aktDeoxyglucoseGastric BypassReceptors, LeptinAdipokinesAdipose Tissue, BrownHemoglobin A, GlycosylatedGene Expression RegulationMuscle ProteinsInsulin, Regular, Human

SecretionTissuesDiabetic ratsHomeostasisSkeletal MuscleDyslipidemiaHumansHyperglycemiaMetabolismResistance and impairedEffects of insulinRosiglitazonePioglitazoneImprove insulin sensitivityRestoresLipolysisFattyAdiponectinObesity-induced insulin resistanceAdiposityEndogenous insulinPostprandial insulinDevelopment of insulin resistanceMetabolic SyndromeDiabetesT2DMMicePeripheral insulinInflammationHyperinsulinemiaConcentrationsLevelsLipid profileWhite adiposMacrophageCytokinesGeneticReductionsPancreaticReceptorResponsiveLiver

Secretion5

• It is known that resveratrol affects insulin secretion and blood insulin concentration. (anti-agingfirewalls.com)
• It is characterized by hyperglycemia and defective production and/or secretion of insulin and complications in the heart, kidney, and neural system leading to death, which have drawn notable attention to the management of diabetes. (frontiersin.org)
• Peripheral CB 1 R blockade, in vivo depletion of macrophages or macrophage-specific knockdown of CB 1 R reverses or prevents these changes and restores normoglycemia and glucose-induced insulin secretion. (nature.com)
• To the best of our knowledge, short-chain fatty acids (SCFAs), bile salt hydrolase (BSH), metabolic endotoxemia and the endocannabinoid (eCB) system are essential in regulating the initiation and progression of MS through the normalization of adipogenesis and the regulation of insulin secretion, fat accumulation, energy homeostasis, and plasma cholesterol levels. (biomedcentral.com)
• GLP-1 is an intestinally-derived peptide that stimulates insulin secretion in response to food intake, as well as reducing the rate of gastric emptying, thus promoting satiety and weight loss. (ddw-online.com)

Tissues9

• PPAR receptors are found in tissues important for insulin action such as adipose tissue, skeletal muscle, and liver. (globalrph.com)
• The metabolic changes produced by pioglitazone result in increased responsiveness of insulin-dependent tissues and are observed in numerous animal models of insulin resistance. (globalrph.com)
• The antidiabetic activity of rosiglitazone has been demonstrated in animal models of type 2 diabetes in which hyperglycemia and/or impaired glucose tolerance is a consequence of insulin resistance in target tissues. (globalrph.com)
• In animal models, the antidiabetic activity of rosiglitazone was shown to be mediated by increased sensitivity to insulin's action in the liver, muscle, and adipose tissues. (globalrph.com)
• Insulin resistance is defined as an inadequate response by insulin target tissues, such as skeletal muscle, liver, and adipose tissue, to the physiologic effects of circulating insulin. (jci.org)
• The hallmarks of impaired insulin sensitivity in these three tissues are decreased insulin-stimulated glucose uptake into skeletal muscle, impaired insulin-mediated inhibition of hepatic glucose production in liver, and a reduced ability of insulin to inhibit lipolysis in adipose tissue. (jci.org)
• Dysregulated autophagy in pancreatic β cells due to hyperglycemia, oxidative stress, and inflammation is associated with diabetes and accompanied by dysregulated autophagy in insulin target tissues and the progression of diabetic complications. (frontiersin.org)
• The purpose of this study was to compare the effects of two training modalities (moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT)) on the pro/antioxidant status of different tissues in obese Zucker rats. (hindawi.com)
• TNF-α is an important pro-inflammatory mediator that contributes to decreased expression of glucose transporter 4 (GLUT4) in adipose, skeletal, and cardiac muscle tissues leading to insulin resistance and T2DM pathogenesis [ 9 ]. (biomedcentral.com)

Diabetic rats4

• Moreover, numerous data indicate that in diabetic rats, resveratrol is able to reduce hyperglycemia. (anti-agingfirewalls.com)
• Figure 3: Macrophage content and Nlrp3 expression in islets of lean and diabetic rats. (nature.com)
• To evaluate this assumption, we investigated the effects of aerobic exercise training (AET), resistance exercise training (RET), and 4 weeks of de-training on serum leptin and TNF-α levels in diabetic rats. (biomedcentral.com)
• These findings indicate that both AET and RET are useful in reducing levels of serum adipocytokines (TNF-α, leptin) in diabetic and non-diabetic rats. (biomedcentral.com)

Homeostasis2

• Alpha-Linolenic Acid Supplementation Prevents Exercise-Induced Improvements in White Adipose Tissue Mitochondrial Bioenergetics and Whole-Body Glucose Homeostasis in Obese Zucker Rats. (uoguelph.ca)
• However, larger, adequately powered, randomized, placebo-controlled, double-blind trials examining multiple measures of carbohydrate and lipid metabolism and insulin homeostasis are needed. (lww.com)

Skeletal Muscle5

• Age-Associated Impairments in Mitochondrial ADP Sensitivity Contribute to Redox Stress in Senescent Human Skeletal Muscle. (uoguelph.ca)
• Controlling CPT-I M-CoA Sensitivity in Skeletal Muscle: The Importance of AMPK-Independent Regulation of Intermediate Filaments During Exercise. (uoguelph.ca)
• We discuss how pathways that "sense" nutrients within skeletal muscle are readily able to regulate insulin action. (jci.org)
• Contractile activity restores insulin responsiveness in skeletal muscle of obese Zucker rats. (ecu.edu)
• Both insulin and contraction stimulate glucose transport in skeletal muscle. (ecu.edu)

Dyslipidemia5

• Abstract Introduction: Dyslipidemia secondary to obesity is a risk factor related to cardiovascular disease events, however a pathological conventional lipid profile (CLP) is infrequently found in obese children. (biosferteslab.com)
• Type 2 diabetes is a complex metabolic disorder characterized by hyperglycemia, impaired glucose tolerance and insulin resistance associated with dyslipidemia and hypertension. (biomedcentral.com)
• This altered glucose metabolism state is associated with an increased risk of developing T2DM (Figure 1), although other parameters including excess adiposity, inflammation and dyslipidemia are risk factors associated with the development of insulin resistance, loss of pancreatic function, worsening of hyperglycemia and progression to diabetes (1). (ddw-online.com)
• Replacement of GH in adults with GHD markedly reduces central obesity and substantially reduces total cholesterol levels but has produced little change in other risk factors, particularly insulin resistance and dyslipidemia. (medscape.com)
• [ 13 ] For these patients, concerns are the persistent insulin resistance and dyslipidemia, together with the elevated plasma insulin and lipoprotein(a) levels observed with GH replacement. (medscape.com)

Humans5

• Expression of NLRP3 inflammasome and T cell population markers in adipose tissue are associated with insulin resistance and impaired glucose metabolism in humans. (nature.com)
• Insulin-stimulated glucose transport is decreased in obese humans and rats. (ecu.edu)
• Blood levels of the BCAAs are elevated in obese, insulin resistant humans and in mouse and rat models of diet-induced diabetes, suggesting the possibility that BCAAs contribute to the pathogenesis of obesity and diabetes. (wikipedia.org)
• were the first to demonstrate in obese mice and in humans with obesity that fat accumulation is positively associated with systemic oxidative stress, suggesting that the oxidative stress increase in people with obesity could be explained by reactive oxygen species (ROS) overproduction in adipose tissue [ 17 ]. (hindawi.com)
• The relation between cerebrospinal fluid and serum levels of leptin in obese humans (17,18) suggests that defective BBB transport accounts for more of the overall resistance to leptin than the receptor/postreceptor defects (19). (clubalthea.com)

Hyperglycemia2

• In animal models of diabetes, pioglitazone reduces the hyperglycemia, hyperinsulinemia, and hypertriglyceridemia characteristic of insulin-resistant states such as type 2 diabetes. (globalrph.com)
• Type 2 diabetes mellitus (T2DM) progresses from compensated insulin resistance to beta cell failure resulting in uncompensated hyperglycemia, a process replicated in the Zucker diabetic fatty (ZDF) rat. (nature.com)

Metabolism4

• Sodium Nitrate Supplementation Alters Mitochondrial H 2 O 2 Emission but Does Not Improve Mitochondrial Oxidative Metabolism in the Heart of Healthy Rats. (uoguelph.ca)
• Activation of PPARγ nuclear receptors modulates the transcription of a number of insulin responsive genes involved in the control of glucose and lipid metabolism. (globalrph.com)
• Secondary endpoints included resting energy expenditure (REE), plasma metabolites, and glucose and insulin metabolism as assessed by a frequently sampled intravenous glucose tolerance test.RESULTS Chronic mirabegron therapy increased BAT metabolic activity. (jci.org)
• In a study of 60 women with polycystic ovary syndrome, taking a flaxseed omega-3 supplement twice daily for 12 weeks improved insulin metabolism and cholesterol levels with little effect on hormone levels and lipid levels. (earthtokathy.com)

Resistance and impaired1

• Type 2 DM is a heterogeneous, progressive disorder initially characterized by impaired glucose tolerance and compensatory hyperinsulinemia, which in the later stages, develops severe insulin resistance and impaired beta cell function [ 2 , 3 ]. (biomedcentral.com)

Effects of insulin1

• 0.05) and a 52% increase in the sensitivity of peripheral adipocytes to the inhibitory effects of insulin on lipolysis ( P = 0.04). (diabetesjournals.org)

Rosiglitazone4

• We examined the effect of three months of rosiglitazone treatment (4 mg b.i.d.) on whole-body insulin sensitivity and in vivo peripheral adipocyte insulin sensitivity as assessed by glycerol release in microdialysis from subcutaneous fat during a two-step (20 and 120 mU · m −2 · min −1 ) hyperinsulinemic-euglycemic clamp in nine type 2 diabetic subjects. (diabetesjournals.org)
• Rosiglitazone, a member of the thiazolidinedione class of antidiabetic agents, improves glycemic control by improving insulin sensitivity. (globalrph.com)
• Rosiglitazone reduces blood glucose concentrations and reduces hyperinsulinemia in the ob/ob obese mouse, db/db diabetic mouse, and fa/fa fatty Zucker rat. (globalrph.com)
• PPAR-gamma agonists, also known as thiazolidinediones (TZDs), such as Pioglitazone and Rosiglitazone increase insulin sensitivity, reduce levels of blood glucose, insulin and triglycerides with a concomitant reduction in BP and improvement in endothelial function [ 8 , 9 ]. (biomedcentral.com)

Pioglitazone6

• CONCLUSIONS -These results suggest that pioglitazone therapy in type 2 diabetic patients decreases fasting and postprandial plasma glucose levels by improving hepatic and peripheral (muscle) tissue sensitivity to insulin. (diabetesjournals.org)
• Unlike sulfonylureas, pioglitazone is not an insulin secretagogue. (globalrph.com)
• The present study examined the combined effects of an antihypertensive (S-Amlodipine) and an insulin-sensitizing agent, peroxisome proliferator-activated receptor (PPAR) agonists (Pioglitazone and Ragaglitazar), on cardiovascular risk factors in aged diabetic and insulin-resistant Zucker fa/fa rats. (biomedcentral.com)
• In combination, S-Amlodipine and Pioglitazone significantly reduced blood glucose (115.1 ± 6.6 vs. 81.7 ± 4.2), BP (184.4 ± 5.0 vs. 155.1 ± 5.0), serum triglycerides (362.5 ± 47.5 vs. 211.1 ± 23.7) and glucose intolerance when compared with vehicle treated Zucker fa/fa rats. (biomedcentral.com)
• Furthermore, there was less body weight gain and food intake with S-Amlodipine and Pioglitazone combination in Zucker fa/fa rats. (biomedcentral.com)
• Current widespread treatments for T2DM include metformin (suppressor of hepatic glucose production), sulfonylureas (insulin secretagogues), and the thiazolidinedione pioglitazone (PPAR agonist). (ddw-online.com)

Improve insulin sensitivity1

• A wealth of published data documents the ability of carnitine to improve insulin sensitivity, mitochondrial function, and cardiovascular health. (lifeextension.com)

Restores1

• BCAA-restricted diets improve glucose tolerance and promote leanness in normal weight mice, restores insulin sensitivity and normal body weight to obese mice and promotes insulin sensitivity in obese rats. (wikipedia.org)

Lipolysis1

• Encouraging preclinical results suggest that β3-AR agonists could also improve obesity-related metabolic disease by increasing brown adipose tissue (BAT) thermogenesis, white adipose tissue (WAT) lipolysis, and insulin sensitivity.METHODS We treated 14 healthy women of diverse ethnicities (27.5 ± 1.1 years of age, BMI of 25.4 ± 1.2 kg/m2) with 100 mg mirabegron (Myrbetriq extended-release tablet, Astellas Pharma) for 4 weeks in an open-label study. (jci.org)

Fatty4

• In conclusion, these results support the hypothesis that thiazolidinediones enhance insulin sensitivity in patients with type 2 diabetes by promoting increased insulin sensitivity in peripheral adipocytes, which results in lower plasma fatty acid concentrations and a redistribution of intracellular lipid from insulin responsive organs into peripheral adipocytes. (diabetesjournals.org)
• Can Dietary Omega-3 Fatty Acid Supplementation Reduce Inflammation in Obese Pregnant Women: A Discussion of a Randomized Double-Blind Controlled Clinical Trial. (earthtokathy.com)
• We then discuss how obesity leads to insulin resistance via a complex interplay among systemic fatty acid excess, microhypoxia in adipose tissue, ER stress, and inflammation. (jci.org)
• Endocannabinoids May Mediate the Ability of (n-3) Fatty Acids to Reduce Ectopic Fat and Inflammatory Mediators in Obese Zucker Rats. (rejuvenation-science.com)

Adiponectin2

• Bone marrow adipose tissue (MAT) contributes to increased circulating adiponectin, an insulin-sensitizing hormone, during caloric restriction (CR), but whether this occurs in other contexts remains unknown. (frontiersin.org)
• In non-obese subjects, adipocytes release higher levels of adiponectin that improves insulin sensitivity and enhances M2 macrophage polarization [ 15 ]. (biomedcentral.com)

Obesity-induced insulin resistance1

• The Nlrp3 inflammasome has been implicated in obesity-induced insulin resistance and beta cell failure. (nature.com)

Adiposity4

• In some studies, resveratrol was reported to reduce body weight and adiposity in obese animals. (anti-agingfirewalls.com)
• HFD-associated postprandial insulin resistance is largely mediated by impairment of parasympathetic-dependent insulin action, which correlates with adiposity. (ibict.br)
• Figure 1: Effects of peripheral CB 1 R blockade on body weight, adiposity, hepatic lipogenesis and glycemic control in ZDF rats. (nature.com)
• The exact actions of PPARbeta/delta are still being researched, though in obese animals it appears to decrease adiposity. (bodybuilding.com)

Endogenous insulin1

• Due to its mechanism of action, AVANDIA is active only in the presence of endogenous insulin. (healthyplace.com)

Postprandial insulin2

• High-fat diet results in postprandial insulin resistance that involves parasympathetic dysfunctionParasympatheticnitric-oxidevisceraladipositypostmealadipose-tissueobesenervesskeletal-musclewhiteblockadeoxidativeHigh-fatdietzuckerObesitystressglucoserattestInsulinristresistancenervous-systemsynthasesensitivityObesityHigh-fat dietInsulin resistanceParasympathetic nervesSDG 3 - Good Health and Well-beingWe are indebted to Dr Zhi Ming for sharing technical expertise and Gerald Nolette from the Central Animal Care Services of the University of Manitoba for animal care assistance. (ibict.br)
• In conclusion, fat accumulation induced by HFD is associated with postprandial insulin resistance, but not with fasting insulin resistance. (ibict.br)

Development of insulin resistance1

• TGF-β, especially TGF-β1 as an uppermost isoform of TGF-β superfamily, may play a very essential role in the development of insulin resistance and obesity and finally, diabetes. (frontiersin.org)

Metabolic Syndrome1

• The aim of this study was to evaluate acylated ghrelin and obestatin levels and their ratio in obese and normal-weight children and adolescents, and their association with metabolic syndrome (MetS) parameters. (mdpi.com)

Diabetes8

• Insulin resistance is a common feature characterizing the pathogenesis of type 2 diabetes. (globalrph.com)
• Taking CLA by mouth does not improve pre-meal or post-meal blood sugar or insulin levels in people with type 2 diabetes . (webmd.com)
• Insulin resistance is a major metabolic feature of obesity and is a key factor in the etiology of a number of diseases, including type 2 diabetes. (jci.org)
• Another pathway, TGF-β signaling pathway, appears to play a part in the progression of diabetes, insulin resistance, and autoimmunity in both type 1 and 2 diabetes and complications in diabetes. (frontiersin.org)
• This can lead to a reduced insulin sensitivity and contribute to the development of type 2 diabetes. (rejuvenation-science.com)
• Clinical studies suggest that type 2 diabetes mellitus (T2DM) is a risk factor for cognitive decline and dementia, and have found evidence that insulin resistance (IR) occurs in the brain of patients with T2DM and Alzheimer disease (AD). (nature.com)
• Clinical studies suggest a link between type 2 diabetes mellitus (T2DM) and insulin resistance (IR) and cognitive dysfunction, but there are significant gaps in our knowledge of the mechanisms underlying this relationship. (nature.com)
• A common risk factor in diabetes is insulin resistance caused by high-fat diet (HFD) in obese people [ 7 ]. (biomedcentral.com)

T2DM2

• Importantly, both lifestyle (diet and exercise) and pharmacological interventions that are known to alleviate peripheral IR effectively restore hippocampal neuroplasticity in rodent models of T2DM and AD, and this effect may be due to restoration of insulin signalling in the hippocampus. (nature.com)
• This Review highlights these observations and discusses intervention studies which suggest that the restoration of insulin activity in the hippocampus may be an effective strategy to alleviate the cognitive decline associated with T2DM and AD. (nature.com)

Mice3

• In lean and obese mice, these benefits of BCAA-restriction are mediated by isoleucine and valine, and not by restriction of leucine. (wikipedia.org)
• Second, an unidentified mechanism impairs transport in obese mice even when BBB transport is assessed by brain perfusion, a method that removes the immediate effects of blood-borne substances. (clubalthea.com)
• The inability of obese mice to respond to peripherally administered leptin while responding to centrally administered leptin is likely caused by a defect in leptin transport across the BBB. (clubalthea.com)

Peripheral insulin1

• and hepatic and peripheral insulin sensitivity was measured with a two-step euglycemic insulin (40 and 160 mU · min − 1 · m -2 ) clamp performed with 3-[ 3 H]glucose and indirect calorimetry. (diabetesjournals.org)

Inflammation3

• In the past, numerous studies investigating WAT inflammation have shown that the release of pro-inflammatory cytokines, such as TNFα, IL-6 or gp130 cytokines, are implicated in insulin-resistance [ 9 , 10 ]. (springer.com)
• In particular, we focus on the hypothesis that the macrophage is an important cell type in the propagation of inflammation and induction of insulin resistance in obesity. (jci.org)
• Adipose tissue extension is also associated with enhanced adipose tissue inflammation and hypoxia, promoting recruitment of pro-inflammatory macrophages that secrete cytokines, such as tumor necrosis factor (TNF-α) and Interleukin 6 (IL-6), which, by activating the TNF-α receptor and other cytokine receptors, they worsen insulin resistance [ 8 ]. (biomedcentral.com)

Hyperinsulinemia1

• In animals with hyperinsulinemia, resveratrol was found to reduce blood insulin. (anti-agingfirewalls.com)

Concentrations1

• 0.01) decreased significantly without change in fasting or glucose-stimulated insulin/C-peptide concentrations. (diabetesjournals.org)

Levels4

• 0.01), reduced hemoglobin A1c levels (P = 0.01), and improved insulin sensitivity (P = 0.03) and β cell function (P = 0.01). (jci.org)
• In the presence of a robust compensatory insulin secretory response to insulin resistance, glucose levels can remain relatively normal. (jci.org)
• serum aminotransferases, inflammatory cytokines (IL-6 and TNF-α), glucose and insulin levels. (p450inhibitors.com)
• Serum insulin, leptin, and TNF-α levels were assessed by commercial ELISA kits. (biomedcentral.com)

Lipid profile1

• For years, moderate-intensity continuous training (MICT) has been the most popular exercise modality for improving body composition, cardiorespiratory fitness, insulin resistance, and lipid profile [ 2 , 5 ]. (hindawi.com)

White adipos1

• Recently, we and others have demonstrated fibrotic depots in white adipose tissue of obese subjects. (springer.com)

Macrophage3

• Figure 4: Effects of macrophage depletion on glycemic control and proinflammatory signaling in islets of ZDF rats. (nature.com)
• Figure 5: Effects of macrophage-selective siRNA knockdown of CB 1 R in ZDF rats. (nature.com)
• The objective of this study was to evaluate the relationship between TREM-1 and macrophage polarization, and association of TREM-1 and M1 macrophage polarization with insulin resistance (IR) in obese population compared to non-obese population. (biomedcentral.com)

Cytokines1

• The imbalance in obese patients due to pro-inflammatory cytokines influences the M1/M2 polarization. (biomedcentral.com)

Genetic2

• The causes of insulin resistance can be genetic and/or acquired. (jci.org)
• Nonetheless, it is likely that any genetic component must interact with environmental factors in order for insulin resistance to develop into a pathophysiologically meaningful abnormality. (jci.org)

Reductions1

• Exercise-Induced Reductions in Mitochondrial ADP Sensitivity Contribute to the Induction of Gene Expression and Mitochondrial Biogenesis Through Enhanced Mitochondrial H 2 O 2 Emission. (uoguelph.ca)

Pancreatic1

• Here we show that beta cell failure in adult ZDF rats is not associated with CB 1 R signaling in beta cells, but rather in M1 macrophages infiltrating into pancreatic islets, and that this leads to activation of the Nlrp3-ASC inflammasome in the macrophages. (nature.com)

Receptor1

• Figure 3: Insulin receptor signalling in the hippocampus. (nature.com)

Responsive1

• Activation of PPARγ nuclear receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. (globalrph.com)

Liver3

• ACTOS decreases insulin resistance in the periphery and in the liver resulting in increased insulin-dependent glucose disposal and decreased hepatic glucose output. (globalrph.com)
• The results of our study showed over-expression of TREM-1, M1 markers and down-regulation of TREM-2 and M2 markers in the omentum, subcutaneous and liver biopsies of obese patients (diabetics and non-diabetics) compared to non-obese patients. (biomedcentral.com)
• TREM-1 expression is significantly increased along with the M1 markers in liver biopsy of obese diabetic (17/17) and obese non-diabetic patients (9/16). (biomedcentral.com)