Association between cognitive impairment patient with solid cancer and insulin resistance

Abstract Objectives In an aging population, an increase in the number of elderly cancer patients with cognitive impairment is expected. The possible association between cancer and cognitive impairment is important to elucidate, because it can have a serious impact on quality of life. Here, we focused on glucose metabolism as a factor that links cancer and cognitive impairment. Results Thirteen subjects with solid cancers and cognitive impairment were recruited. As a control group, 14 subjects with cognitive impairment alone and 8 subjects with cancer alone were recruited. A Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and that of β-cell function (HOMA-B) were used. In comparison with patients with solid cancer alone, those with cognitive impairment alone and those with both cancer and cognitive impairment had increased HOMA-IR values. Insulin resistance was increased in patients with cognitive impairment alone and those with both cognitive impairment and solid cancer than in patients without cognitive impairment; however, β-cell function was not affected. The present data indicated that elderly cancer patients with high HOMA-IR score may be at a relatively high risk for developing cognitive impairment. Furthermore, early treatment to reduce insulin sensitivity may prevent cognitive impairment.

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Association between cognitive impairment patient with solid cancer and insulin resistance

10.21203/rs.2.13344/v3 ◽

2019 ◽

Author(s):

Kenji Gonda ◽

Kenji Yaginuma ◽

Yuichi Rokkaku ◽

Shoichiro Horita ◽

Yuko Maejima ◽

...

Keyword(s):

Insulin Resistance ◽

Cognitive Impairment ◽

Cancer Patients ◽

Cell Function ◽

Control Group ◽

Solid Cancer ◽

Model Assessment ◽

Β Cell ◽

Elderly Cancer Patients ◽

Β Cell Function

Abstract Objectives In an aging population, an increase in the number of elderly cancer patients with cognitive impairment is expected. The possible association between cancer and cognitive impairment is important to elucidate, because it can have a serious impact on quality of life. Here, we focused on glucose metabolism as a factor that links cancer and cognitive impairment. Results Thirteen subjects with solid cancers and cognitive impairment were recruited. As a control group, 14 subjects with cognitive impairment alone and 8 subjects with cancer alone were recruited. A Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and that of β-cell function (HOMA-B) were used. In comparison with patients with solid cancer alone, those with cognitive impairment alone and those with both cancer and cognitive impairment had increased HOMA-IR values. Insulin resistance was increased in patients with cognitive impairment alone and those with both cognitive impairment and solid cancer than in patients without cognitive impairment; however, β-cell function was not affected. The present data indicated that elderly cancer patients with high HOMA-IR score may be at a relatively high risk for developing cognitive impairment. Furthermore, early treatment to reduce insulin sensitivity may prevent cognitive impairment.

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Association between cognitive impairment patient with solid cancer and insulin resistance

10.21203/rs.2.13344/v4 ◽

2019 ◽

Author(s):

Kenji Gonda ◽

Kenji Yaginuma ◽

Yuichi Rokkaku ◽

Shoichiro Horita ◽

Yuko Maejima ◽

...

Keyword(s):

Insulin Resistance ◽

Cognitive Impairment ◽

Cancer Patients ◽

Cell Function ◽

Control Group ◽

Solid Cancer ◽

Model Assessment ◽

Β Cell ◽

Elderly Cancer Patients ◽

Β Cell Function

Abstract Objectives In an aging population, an increase in the number of elderly cancer patients with cognitive impairment is expected. The possible association between cancer and cognitive impairment is important to elucidate, because it can have a serious impact on quality of life. Here, we focused on glucose metabolism as a factor that links cancer and cognitive impairment. Results Thirteen subjects with solid cancers and cognitive impairment were recruited. As a control group, 14 subjects with cognitive impairment alone and 8 subjects with cancer alone were recruited. A Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and that of β-cell function (HOMA-B) were used. In comparison with patients with solid cancer alone, those with cognitive impairment alone and those with both cancer and cognitive impairment had increased HOMA-IR values. Insulin resistance was increased in patients with cognitive impairment alone and those with both cognitive impairment and solid cancer than in patients without cognitive impairment; however, β-cell function was not affected. The present data indicated that elderly cancer patients with high HOMA-IR score may be at a relatively high risk for developing cognitive impairment. Furthermore, early treatment to reduce insulin sensitivity may prevent cognitive impairment.

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Patients with both cognitive impairment and solid cancer present increased insulin resistance

10.21203/rs.2.13344/v1 ◽

2019 ◽

Author(s):

Kenji Gonda ◽

Kenji Yaginuma ◽

Yuichi Rokkaku ◽

Shoichiro Horita ◽

Yuko Maejima ◽

...

Keyword(s):

Insulin Resistance ◽

Cognitive Impairment ◽

Cancer Patients ◽

Cell Function ◽

Solid Cancer ◽

Model Assessment ◽

Β Cell ◽

Elderly Cancer Patients ◽

Significant Difference ◽

Β Cell Function

Abstract Objective In an aging population, an increase in elderly cancer patients with cognitive impairment is to be expected. Because cognitive impairment has a serious impact on quality of life of cancer patients, it is important to elucidate the possible association between cancer and cognitive impairment. Here, we focused on glucose metabolism as a factor that links cancer and cognitive impairment. Results A homeostasis model assessment was used to assess insulin resistance (HOMA-IR) and β-cell function (HOMA-B). HOMA-B showed no difference among patients with cancer, with dementia, and with both. However, there was a significant difference in HOMA-IR. In comparison with patients with only solid cancer, patients with only cognitive impairment and those with both cancer and cognitive impairment showed increased HOMA-IR value. Insulin resistance was increased in patients with cognitive impairment only and those with both cognitive impairment and solid cancer compared to cancer patients without cognitive impairment; however, β-cell function was not affected. The present data indicate that elderly cancer patients with a high HOMA-IR score may be in higher risk of developing cognitive impairment. Furthermore, early treatment to reduce insulin sensitivity may become the prevention of cognitive impairment.

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Study on the correlation between the changes of TNFR1, TNF-α, and adiponectin in patients with gestational diabetes mellitus and insulin resistance

European Journal of Inflammation ◽

10.1177/2058739219846346 ◽

2019 ◽

Vol 17 ◽

pp. 205873921984634

Author(s):

Jie Xie ◽

Lan Dai ◽

Xiaolei Tang

Keyword(s):

Insulin Resistance ◽

Research Group ◽

Cell Function ◽

Control Group ◽

Model Assessment ◽

Homeostasis Model Assessment ◽

Β Cell ◽

Tnf Α ◽

Β Cell Function ◽

Necrosis Factor

Gestational diabetes mellitus (GDM) refers to pregnant women with impaired glucose tolerance, which could bring high risk to the mother and fetus. However, the early diagnosis and treatment of GDM remained unclear. In this study, 60 patients with GDM were selected as the research group and 50 healthy pregnant women as the control group. Tumor necrosis factor receptor 1 (TNFR1), tumor necrosis factor-α (TNF-α), and adiponectin (ADP) in the serum were measured by enzyme-linked immunosorbent assays (ELISAs). The levels of fasting blood glucose (FBG), fasting insulin (FINS), and glycosylated hemoglobin (HbA1c) were also detected to calculate homeostasis model assessment insulin resistance index (HOMA-IR) and pancreatic β-cell function index (HOMA-HBCl). Compared with the control group, the serum levels of TNFR1, TNF-α, and HbA1c in research group were significantly increased ( P < 0.05), while ADP showed lower levels ( P < 0.01). Furthermore, FBG, FINS, and HOMA-IR were evidently increased ( P < 0.05), while homeostasis model assessment insulin secretion index (HOMA-β) and insulin sensitivity index (ISI) were decreased ( P < 0.05) in research group. TNFR and TNF-α were positively correlated with FBG, FINS, and HOMA-IR ( P < 0.05). In addition, there was a significant negative correlation between ADP and FINS and HOMA-IR ( P < 0.01). From logistic regression analysis, age, gestational age, FBG, FINS, TNFR1, TNF-α, and ADP ( P < 0.05) were shown to be risk factors to affect the function of islet β-cells. In conclusion, the high levels of TNFR1 and TNF-α and the low levels of ADP in the second trimester of pregnancy are the risk factors of GDM, which are related to the insulin resistance and impaired pancreatic β-cell function.

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Estimates of Insulin Secretory Function in Apparently Healthy Volunteers Vary as a Function of How the Relevant Variables Are Quantified

Clinical Chemistry ◽

10.1373/clinchem.2010.152744 ◽

2011 ◽

Vol 57 (4) ◽

pp. 627-632 ◽

Cited By ~ 5

Author(s):

Barry R Johns ◽

Fahim Abbasi ◽

Gerald M Reaven

Keyword(s):

Insulin Resistance ◽

Insulin Secretion ◽

Plasma Glucose ◽

Insulin Action ◽

Cell Function ◽

Model Assessment ◽

Pancreatic Β Cell ◽

Homeostasis Model Assessment ◽

Β Cell ◽

Β Cell Function

BACKGROUND Several surrogate estimates have been used to define relationships between insulin action and pancreatic β-cell function in healthy individuals. Because it is unclear how conclusions about insulin secretory function depend on specific estimates used, we evaluated the effect of different approaches to measurement of insulin action and secretion on observations of pancreatic β-cell function in individuals whose fasting plasma glucose (FPG) was <7.0 mmol/L (126 mg/dL). METHODS We determined 2 indices of insulin secretion [homeostasis model assessment of β-cell function (HOMA-β) and daylong insulin response to mixed meals], insulin action [homeostasis model assessment of insulin resistance (HOMA-IR) and steady-state plasma glucose (SSPG) concentration during the insulin suppression test], and degree of glycemia [fasting plasma glucose (FPG) and daylong glucose response to mixed meals] in 285 individuals with FPG <7.0 mmol/L. We compared the relationship between the 2 measures of insulin secretion as a function of the measures of insulin action and degree of glycemia. RESULTS Assessment of insulin secretion varied dramatically as a function of which of the 2 methods was used and which measure of insulin resistance or glycemia served as the independent variable. For example, the correlation between insulin secretion (HOMA-β) and insulin resistance varied from an r value of 0.74 (when HOMA-IR was used) to 0.22 (when SSPG concentration was used). CONCLUSIONS Conclusions about β-cell function in nondiabetic individuals depend on the measurements used to assess insulin action and insulin secretion. Viewing estimates of insulin secretion in relationship to measures of insulin resistance and/or degree of glycemia does not mean that an unequivocal measure of pancreatic β-cell function has been obtained.

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Flaxseed oil prevents trans-10, cis-12-conjugated linoleic acid-induced insulin resistance in mice

British Journal Of Nutrition ◽

10.1017/s0007114508027451 ◽

2008 ◽

Vol 101 (5) ◽

pp. 701-708 ◽

Cited By ~ 34

Author(s):

Darshan S. Kelley ◽

Madhuri Vemuri ◽

Yuriko Adkins ◽

Sher Himmat S. Gill ◽

Dawn Fedor ◽

...

Keyword(s):

Insulin Resistance ◽

Linoleic Acid ◽

Conjugated Linoleic Acid ◽

Cell Function ◽

Flaxseed Oil ◽

Control Group ◽

Β Cell ◽

Liver Lipids ◽

Alcoholic Fatty Liver ◽

Β Cell Function

Insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) are found in 35 and 30 % of US adults, respectively. Trans-10, cis-12-conjugated linoleic acid (CLA) has been found to cause both these disorders in several animal models. We hypothesised that IR and NAFLD caused by CLA result from n-3 fatty acid deficiency. Pathogen-free C57BL/6N female mice (aged 8 weeks; n 10) were fed either a control diet or diets containing trans-10, cis-12-CLA (0·5 %) or CLA+flaxseed oil (FSO) (0·5 %+0·5 %) for 8 weeks. Weights of livers, concentration of circulating insulin, values of homeostatic model 1 (HOMA1) for IR and HOMA1 for β cell function were higher by 160, 636, 985 and 968 % in the CLA group compared with those in the control group. FSO decreased fasting glucose by 20 % and liver weights by 37 % compared with those in the CLA group; it maintained circulating insulin, HOMA1-IR and HOMA1 for β cell function at levels found in the control group. CLA supplementation decreased n-6 and n-3 wt% concentrations of liver lipids by 57 and 73 % and increased the n-6:n-3 ratio by 58 % compared with corresponding values in the control group. FSO increased n-6 and n-3 PUFA in liver lipids by 33 and 342 % and decreased the n-6:n-3 ratio by 70 % compared with corresponding values in the CLA group. The present results suggest that some adverse effects of CLA may be due to n-3 PUFA deficiency and that these can be corrected by a concomitant increase in the intake of α-linolenic acid, 18 : 3n-3.

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Insulin Resistance and Beta Cell Dysfunction in Severe Falciparum Malaria with Multi Organ Dysfunction Syndrome (MODS)

Volume 5 - 2020, Issue 9 - September - International Journal of Innovative Science and Research Technology ◽

10.38124/ijisrt20aug309 ◽

2020 ◽

Vol 5 (8) ◽

pp. 1756-1759

Author(s):

Manoj Kumar Mohapatra ◽

Muralidhar Anantrao Sangle ◽

Prafulla Kumar Bariha

Keyword(s):

Insulin Resistance ◽

Falciparum Malaria ◽

Organ Dysfunction ◽

Cell Function ◽

Model Assessment ◽

Homeostasis Model Assessment ◽

Β Cell ◽

Cell Dysfunction ◽

Β Cell Function ◽

Severe Falciparum Malaria

Insulin Resistance is a major factor among patients with critical illness due to various causes. Severe falciparum malaria with MODS diagnosed as per the criteria of MSS and admitted to the Medical ward of our hospital were assessed for IR and β cell function by using homeostasis model assessment. 75 consecutive patients of SFM admitted to the Medical ward of our hospital were included in this study. Malaria was diagnosed as per criteria of WHO and organ dysfunction was diagnosed as per Malaria Severity Score. Insulin Resistance and β cell function was assessed by using homeostasis model assessment on Day-1 and Day-7. Out of 75 patients of severe falciparum malaria with MODS 2, 3, 4, and 5 organ dysfunctions constituted 16 (21.3%), 34 (45.3%), 16 (21.3%), and 9 (12.0%) patients, respectively.Hepatic failure was the most common organ system failure (n=58; 77.3%), followed by neurological (n=50;66.6%) ,renal (n=40;53.3%), hematological (n=30; 40.0%), and, respiratory failure ( n=15; 20.0%). Hyperglycemia was present in 25 (33.3%) cases where as normoglycemia was present in 50 (66.6%) cases. The values of FBS, Tg, insulin, IR, and β cell function decreased on Day-7 compared to Day-1 after recovery from critically ill state. The patients who died had a high insulin value, IR, but low β cell dysfunction compared to the survivors. This study showed that IR and β cell dysfunction were associated with severe malaria with MODS with increased mortality.

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Large birth size, infancy growth pattern, insulin resistance and β-cell function

Acta Endocrinologica ◽

10.1530/eje-20-1332 ◽

2021 ◽

Author(s):

Rong Huang ◽

Yu Dong ◽

Anne Monique Nuyt ◽

Emile Levy ◽

Shu-Qin Wei ◽

...

Keyword(s):

Insulin Resistance ◽

Beta Cell ◽

Gestational Age ◽

Growth Pattern ◽

Beta Cell Function ◽

Cell Function ◽

Birth Size ◽

Model Assessment ◽

Β Cell ◽

Β Cell Function

Objective: Large birth size programs an elevated risk of type 2 diabetes in adulthood, but data are absent concerning glucose metabolic health impact in infancy. We sought to determine whether large birth size is associated with insulin resistance and β-cell function in infancy, and evaluate the determinants. Design and Participants: In the Canadian 3D birth cohort, we conducted a nested matched (1:2) study of 70 large-for-gestational-age (LGA, birth weight >90th percentile) and 140 optimal-for-gestational-age (OGA, 25th-75th percentiles) control infants. The primary outcomes were homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β) at age 2-years. Results: HOMA-IR and HOMA-β were similar in LGA and OGA infants. Adjusting for maternal and infant characteristics, decelerated growth in length during early infancy (0-3 months) was associated a 25.8% decrease (95% confidence intervals 6.7-41.0%) in HOMA-β. During mid-infancy (3-12 months), accelerated growth in weight was associated with a 25.5% (0.35-56.9%) increase in HOMA-IR, in length with a 69.3% increase (31.4-118.0%) in HOMA-IR and a 24.5% (0.52-54.3%) increase in HOMA-β. Decelerated growth in length during late infancy (1-2 years) was associated with a 28.4% (9.5-43.4%) decrease in HOMA-IR and a 21.2% (3.9-35.4%) decrease in HOMA-β. Female sex was associated with higher HOMA-β, Caucasian ethnicity with lower HOMA-IR, and maternal smoking with lower HOMA-β. Conclusions: The study is the first to demonstrate that large birth size is not associated with insulin resistance and β-cell function in infancy, but infancy growth pattern matters. Decelerated infancy growth may be detrimental to beta-cell function.

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Σύγκριση πλειοτροπικών δράσεων υπολιπιδαιμικών θεραπειών

10.12681/eadd/39629 ◽

2015 ◽

Author(s):

Ελισάβετ Μουτζούρη

Keyword(s):

Insulin Resistance ◽

Phospholipase A2 ◽

Cell Function ◽

Oxidized Ldl ◽

Model Assessment ◽

Pla2 Activity ◽

Homeostasis Model Assessment ◽

Β Cell ◽

Prostaglandin F2 Alpha ◽

Β Cell Function

Εισαγωγή: Οι στατίνες διαθέτουν δράσεις, οι οποίες είναι ανεξάρτητες τηςυπολιπιδαιμικής τους δράσης. Σε αυτές συμπεριλαμβάνονται κυρίως αντιφλεγμονώδεις καιαντιοξειδωτικές δράσεις, καθώς επίσης και επιδράσεις στο μεταβολισμό τους ουρικούοξέος και στο μεταβολισμό της γλυκόζης.Σκοπός: Σκοπός αυτής της διδακτορικής διατριβής ήταν η σύγκριση των επιδράσεωνδιαφορετικών στατινών ή του συνδυασμού μιας στατίνης με την εζετιμίμπη, με τις ίδιεςυπολιπιδαιμικές δράσεις, σε παραμέτρους του οξειδωτικού stress, της φλεγμονής καθώςκαι παραμέτρους του μεταβολισμού του ουρικού οξέους και του μεταβολισμού τηςγλυκόζης σε υπερχοληστερολαιμικούς ασθενείς.Μέθοδοι: Πρωτόκολλο 1 Στη μελέτη συμμετείχαν 153 υπερχοληστερολαιμικοίασθενείς που τυχαιοποιήθηκαν σε σιμβαστατίνη 40 mg ή σε σιμβαστατίνη/εζετιμίμπη10/10 mg ή σε ροσουβαστατίνη 10 mg ημερησίως.Μετρήσαμε (πριν και μετά από 12 εβδομάδες θεραπείας):- Παραμέτρους του οξειδωτικού stress:1) 8-Epi prostaglandin F2 alpha (8-epiPGF2a)2) Oxidized LDL (oxLDL)- Παραμέτρους της φλεγμονής:1) Lipoprotein associated phospholipase A2 (Lp-PLA2) activity and mass- Παραμέτρους του μεταβολισμού της γλυκόζης:1) Homeostasis model assessment of insulin resistance (HOMA-IR)2) Ινσουλίνη νηστείας3) Γλυκόζη νηστείας4) Γλυκοζυλιωμένη αιμοσφαιρίνη (HbA1c)5) HOMA of β-cell function (HOMA-B)- Παραμέτρους του μεταβολισμού του ουρικού οξέους:1) Επίπεδα του ουρικού οξέος,2) Κλασματική απέκκριση του ουρικού οξέοςΠρωτόκολλο 2: Στη μελέτη συμμετείχαν 60 ασθενείς που τυχαιοποιήθηκαν σεσιμβαστατίνη 40 mg ή σε σιμβαστατίνη/εζετιμίμπη 10/10 mg ημερησίως.Μετρήσαμε (πριν και μετά από 12 εβδομάδες θεραπείας):1) Τη μεμβρανική έκφραση των TLR2 και TLR4 σε περιφερικά μονοκύτταρα,2) Την επαγώμενη από λιποπολυσακχαρίτη ενδοκυττάρια έκκριση των ιντερλευκινών1β και 6.Αποτελέσματα: Πρωτόκολλο 1: Παρατηρήθηκε μια σημαντική μείωση στα επίπεδαπλάσματος των 8-ισοπροστανίων και της oxLDL σε όλες τις ομάδες [10%, 8% και 6% (p <0.05 σε σύγκριση με τις αρχικές τιμές) και 41%, 40% και 39% (p < 0.001 σε σύγκριση με τιςαρχικές τιμές) για την ομάδα της σιμβαστατίνης, σιμβαστατίνης/εζετιμίμπης καιροσουβαστατίνης, αντίστοιχα]. Σε όλες τις ομάδες παρατηρήθηκε μια σημαντική μείωσητης μάζας και ενεργότητας της Lp-PLA2 (36%, 31% και 38% και 36%, 32% και 32% για τηνομάδα της σιμβαστατίνης, σιμβαστατίνης/εζετιμίμπης και ροσουβαστατίνης, αντίστοιχα, p< 0.001 σε σύγκριση με τις αρχικές τιμές). Δεν παρατηρήθηκαν διαφορές ανάμεσα στιςομάδες.Και οι 3 θεραπείες σχετίστηκαν με σημαντική αύξηση του δείκτη HOMA-IR και τωνεπιπέδων ινσουλίνης νηστείας (p < 0.05 σε σύγκριση με τις αρχικές τιμές). Δενπαρατηρήθηκαν διαφορές ανάμεσα στις ομάδες. Δεν σημειώθηκαν αλλαγές στα επίπεδατης γλυκόζης νηστείας, της HbA1c και του δείκτη HOMA-Β.Σημαντική μείωση των επιπέδων του ουρικού οξέος παρατηρήθηκε σε όλες τιςομάδες (σιμβαστατίνη 40 mg: -5.7%, σιμβαστατίνη/εζετιμίμπη 10/10 mg: -3.8% καιροσουβαστατίνη 10 mg: -3.8%; p<0.05 σε σύγκριση με τις αρχικές τιμές, p=NS για τησύγκριση ανάμεσα στις 3 θεραπευτικές ομάδες). Η κλασματική έκκριση του ουρικού οξέοςαυξήθηκε, ωστόσο στατιστικά μη σημαντικά, σε όλες τις ομάδες (σιμβαστατίνη/εζετιμίμπη10/10 mg: +6.8%, σιμβαστατίνη 40 mg: +6.8% και ροσουβαστατίνη 10 mg: +5.9%). Ημείωση των επιπέδων του ουρικού οξέος συσχετιζόταν με τη με την αύξηση τηςκλασματικής απέκκρισης του ουρικού οξέος. Οι παράμετροι της νεφρικής λειτουργίαςπαρέμειναν αμετάβλητοι σε όλες τις ομάδες.Πρωτόκολλο 2: Οι υπερχοληστερολαιμικοί ασθενείς είχαν υψηλότερα επίπεδα μεμβρανικής έκφρασης TLR2 και TLR4 σε σύγκριση με την ομάδα ελέγχου (p < 0.02). Τόσο ηθεραπεία με σιμβαστατίνη όσο και η θεραπεία με το συνδυασμόσιμβαστατίνης/εζετιμίμπης οδήγησαν σε σημαντική μείωση της έκφρασης των TLR2 και 4 (p< 0.01 σε σύγκριση με τις αρχικές τιμές), χωρίς διαφορές ανάμεσα στις 2 ομάδες. Επιπλέονκαι οι 2 θεραπείες οδήγησαν σε συγκρίσιμες μειώσεις των επιπέδων έκφρασης της LPS-επαγώμενης ιντερλευκίνης-1β και IL-6 (p < 0.05 σε σύγκριση με τις αρχικές τιμές).Συμπεράσματα: Πρωτόκολλο 1: Η σιμβαστατίνη 40 mg, ο συνδυασμόςσιμβαστατίνης/εζετιμίμπης 10/10 mg και η ροσουβαστατίνη 10 mg μειώνουν σημαντικά ταεπίπεδα των 8-ισοπροστανίων, της oxLDL καθώς και τη μάζα και ενεργότητα της Lp-PLA2 σεπαρόμοιο βαθμό.Οι 3 παραπάνω θεραπείες δε διαφέρουν ως προς τις δράσεις τους στο μεταβολισμότης γλυκόζης.Η σιμβαστατίνη 40 mg, ο συνδυασμός σιμβαστατίνης/εζετιμίμπης 10/10 mg και ηροσουβαστατίνη 10 mg μειώνουν συγκρίσιμα τα επίπεδα του ουρικού οξέος.Πρωτόκολλο 2: Η σιμβαστατίνη 40 mg σε σύγκριση με το συνδυασμό σιμβαστατίνηςμε εζετιμίμπη 10/10 mg μείωσαν παρόμοια τα επίπεδα μεμβρανικής έκφρασης των TLR2,TLR4 και την LPS-επαγώμενη ενδοκυττάρια παραγωγή ιντερλευκίνης -1β και -6 σεπεριφερικά μονοκύτταρα υπερχοληστερολαιμικών ασθενών.

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