Acute administration of interleukin-6 does not increase secretion of glucagon-like peptide-1 in mice

Lind, Sara J.; Svendsen, Berit; Balk-Møller, Emilie; Dahlby, Tina; Kuhre, Rune Ehrenreich; Hartmann, Bolette; Mandrup‐Poulsen, Thomas; Deacon, Carolyn F.; Albrechtsen, Nicolai J. Wewer; Holst, Jens J.

doi:10.14814/phy2.13788

Cited by 8 publications

(3 citation statements)

References 34 publications

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“…5), the higher plasma GLP-1 level in the nonsurvivors could not be originated from the higher intestinal GLP-1 production in the non-survivors. Our finding was also corroborated by the report that IL-6 did not stimulate GLP-1 secretion from GLP-1-producing cells or from mouse small intestine [92]. If only considering GLP-1 secretion from the periphery, the higher level of circulating GLP-1 in non-survivors versus survivors remained mysterious.…”

Section: More Severe Neural Damage In Non-survivors Than In Survivorssupporting

confidence: 86%

Central GLP-1 Resistance Induced by Severe Traumatic Brain Injury Was Associated with Persistent Hyperglycemia in Humans

Zhou¹,

DU²,

Tang³

et al. 2023

Neuroendocrinology

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Introduction: Whether central glucagon-like peptide 1 (GLP-1)/GLP-1 receptor system mediated peripheral glucose homeostasis in patients with traumatic brain injury (TBI) is not clear. We aim to determine if plasma GLP-1 level could distinguish the non-survivors from the survivors during the first 14 days after TBI that could prognose 6 months mortality. Methods: Metabolic, inflammatory, and hematological profiles were examined in 73 patients with TBI in neuro-ICU. Factors that discriminate non-survivors from survivors were determined by Two-way ANOVA. Biomarkers associated with mortality were determined by Binary logistic regression and Cox proportional hazard regression. Results: The non-survivors had higher infectious SOFA scores (P<0.001), lower first 3 days’ body temperature (P=0.017), greater chance of cerebral hernia (P=0.048) and decompressive craniectomy (P=0.001) than the survivors. Higher 14-days plasma GLP-1 (P<0.0001), glucose (P=0.002) and IL-6 (P=0.005) levels, in contrast with lower insulin level at days 4-7 (P=0.020) were found in non-survivors than in survivors. Except the survivors had an increased 14-days platelet number (P<0.001), the two groups did not differ in hematological profile and intestinal barrier function. Although GLP-1 correlated closely with IL-6 in both the two groups, it correlated with neither insulin nor glucose in each group. GLP-1 on days 8-10 and IL-6 on days 1-3 were positively, while insulin on days 4-7 was negatively associated with mortality. Conclusion：Persistent higher GLP-1 level in non-survivors over the survivors may present more severe central resistance to endogenous GLP-1 in non-survivors, which may be associated with progressive hyperglycemia with increased mortality in TBI.

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Section: More Severe Neural Damage In Non-survivors Than In Survivorssupporting

confidence: 86%

Central GLP-1 Resistance Induced by Severe Traumatic Brain Injury Was Associated with Persistent Hyperglycemia in Humans

Zhou¹,

DU²,

Tang³

et al. 2023

Neuroendocrinology

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“…Interestingly, the lack of exercise‐induced active GLP‐1 response in NW opposes previous literature in recreationally active males in which 30 minutes of running MICT (65% V̇O 2max ) increased GLP‐1 compared with CTRL [17]. The lack of IL‐6 effects on active GLP‐1 in our data and more recent studies [37, 38] could be accredited to lower post‐exercise IL‐6 concentrations (<14 vs. 100 pg/mL) potentially stemming from shorter duration (60 vs. 90 minutes) and lower intensity (65% V̇O 2max vs. volitional fatigue) exercise bouts [15]. This suggests that these human protocols insufficiently elevate IL‐6 concentrations to thresholds capable of eliciting a GLP‐1 response.…”

Section: Discussioncontrasting

confidence: 70%

Interleukin‐6 is not involved in appetite regulation following moderate‐intensity exercise in males with normal weight and obesity

Bornath

McKie

McCarthy

et al. 2023

Obesity

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ObjectiveIn obesogenic states and after exercise, interleukin (IL)‐6 elevations are established, and IL‐6 is speculated to be an appetite‐regulating mechanism. This study examined the role of IL‐6 on exercise‐induced appetite regulation in sedentary normal weight (NW) males and those with obesity (OB).MethodsNine NW participants and eight participants with OB completed one non‐exercise control (CTRL) and one moderate‐intensity continuous training (MICT; 60 minutes, 65% V̇O2max) session. IL‐6, acylated ghrelin, active peptide tyrosine‐tyrosine3‐36, active glucagon‐like peptide‐1, and overall appetite perceptions were measured fasted, pre exercise, and 30, 90, and 150 minutes post exercise.ResultsFasted IL‐6 concentrations were elevated in OB (p = 0.005, = 0.419); however, increases following exercise were similar between groups (p = 0.934, = 0.000). Acylated ghrelin was lower in OB versus NW (p < 0.017, d > 0.84), and OB did not respond to MICT (p > 0.512, d < 0.44) although NW had a decrease versus CTRL (p < 0.034, d > 0.61). IL‐6 did not moderate/mediate acylated ghrelin release after exercise (p > 0.251). There were no observable effects of MICT on tyrosine‐tyrosine3‐36, glucagon‐like peptide‐1, or overall appetite (p > 0.334, < 0.062).ConclusionsThese results suggest that IL‐6 is not involved in exercise‐induced appetite suppression. Despite blunted appetite‐regulatory peptide responses to MICT in participants with OB, NW participants exhibited decreased acylated ghrelin; however, no differences in appetite perceptions existed between CTRL and MICT or NW and OB.

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“…Mice fed a high-fat diet for 16 weeks displayed a 2-fold increase in basal GLP-1 secretion from colonic cultures ( 50 ). Moreover, interleukin-6 released from white adipose tissue is thought to stimulate L-cell and α-cell GLP-1 production and secretion, subsequently enhancing insulin secretion ( 51-53 ); however, some studies showed a lack of replication of this effect ( 54 , 55 ). In the present study we observed a significant positive association between fasting total GLP-1 as a predictor both of hs-CRP and ALT in children and adolescents with overweight/obesity, surrogate markers of systemic inflammation, and hepatosteatosis ( 35 , 56 ).…”

Section: Discussionmentioning

confidence: 99%

Fasting Plasma GLP-1 Is Associated With Overweight/Obesity and Cardiometabolic Risk Factors in Children and Adolescents

Stinson

Jonsson

Lund

et al. 2021

The Journal of Clinical Endocrinology &Amp; Metabolism

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Context The importance of fasting GLP-1 in altered metabolic outcomes has been questioned. Objective To assess if fasting GLP-1 differs in children and adolescents with overweight/obesity compared to a population-based reference, and whether concentrations predict cardiometabolic risk (CMR) factors. Methods Analyses were based on The Danish Childhood Obesity Data- and Biobank, a cross-sectional study including children and adolescents, 6-19 years old, from an obesity clinic group (n = 1978) and from a population-based group (n = 2334). Fasting concentrations of plasma total GLP-1 and quantitative CMR factors were assessed. The effects of GLP-1 as a predictor of CMR risk outcomes were examined by multiple linear and logistic regression modelling. Results The obesity clinic group had higher fasting GLP-1 concentrations (median 3.3 pmol/L; interquartile range 2.3–4.3) than the population-based group (2.8 pmol/L; 2.1–3.8; P < 2.2E-16). BMI SDS, waist circumference and total body fat percentage were significant predictors of fasting GLP-1 concentrations in boys and girls. Fasting GLP-1 concentrations positively associated with HOMA-IR, fasting values of insulin, hs-CRP, C-peptide, triglycerides, ALT, HbA1c and SDS of diastolic and systolic blood pressure. A 1-SD increase in fasting GLP-1 associated with an increased risk of insulin resistance (Odds ratio [OR] 1.59), dyslipidemia (OR 1.16), increased ALT (OR 1.14), hyperglycemia (OR 1.12) and hypertension (OR 1.12). Conclusions Overweight/obesity in children and adolescents is associated with increased fasting plasma total GLP-1 concentrations, which was predictive of higher cardiometabolic risk factors.

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Acute administration of interleukin-6 does not increase secretion of glucagon-like peptide-1 in mice

Cited by 8 publications

References 34 publications

Central GLP-1 Resistance Induced by Severe Traumatic Brain Injury Was Associated with Persistent Hyperglycemia in Humans

Central GLP-1 Resistance Induced by Severe Traumatic Brain Injury Was Associated with Persistent Hyperglycemia in Humans

Interleukin‐6 is not involved in appetite regulation following moderate‐intensity exercise in males with normal weight and obesity

Fasting Plasma GLP-1 Is Associated With Overweight/Obesity and Cardiometabolic Risk Factors in Children and Adolescents

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