Lipid-induced glucose intolerance is driven by impaired glucose kinetics and insulin metabolism in healthy individuals

Hypertriglyceridemia is associated with an increased risk of type 2 diabetes. We aimed to comprehensively examine the effects of hypertriglyceridemia on major glucose homeostatic mechanisms involved in diabetes progression. In this randomized, cross-over, single-blinded study, two dual-labeled, 3-ho...

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Veröffentlicht in:Metabolism, clinical and experimental clinical and experimental, 2022-09, Vol.134, p.155247-155247, Article 155247
Hauptverfasser: Tricò, Domenico, Mengozzi, Alessandro, Baldi, Simona, Bizzotto, Roberto, Olaniru, Oladapo, Toczyska, Klaudia, Huang, Guo Cai, Seghieri, Marta, Frascerra, Silvia, Amiel, Stephanie A., Persaud, Shanta, Jones, Peter, Mari, Andrea, Natali, Andrea
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container_title Metabolism, clinical and experimental
container_volume 134
creator Tricò, Domenico
Mengozzi, Alessandro
Baldi, Simona
Bizzotto, Roberto
Olaniru, Oladapo
Toczyska, Klaudia
Huang, Guo Cai
Seghieri, Marta
Frascerra, Silvia
Amiel, Stephanie A.
Persaud, Shanta
Jones, Peter
Mari, Andrea
Natali, Andrea
description Hypertriglyceridemia is associated with an increased risk of type 2 diabetes. We aimed to comprehensively examine the effects of hypertriglyceridemia on major glucose homeostatic mechanisms involved in diabetes progression. In this randomized, cross-over, single-blinded study, two dual-labeled, 3-hour oral glucose tolerance tests were performed during 5-hour intravenous infusions of either 20 % Intralipid or saline in 12 healthy subjects (age 27.9 ± 2.6 years, 11 men, BMI 22.6 ± 1.4 kg/m2) to evaluate lipid-induced changes in insulin metabolism and glucose kinetics. Insulin sensitivity, β cell secretory function, and insulin clearance were assessed by modeling glucose, insulin and C-peptide data. Intestinal glucose absorption, endogenous glucose production, and glucose clearance were assessed from glucose tracers. The effect of triglycerides on β-cell secretory function was examined in perifusion experiments in murine pseudoislets and human pancreatic islets. Mild acute hypertriglyceridemia impaired oral glucose tolerance (mean glucose: +0.9 [0.3, 1.5] mmol/L, p = 0.008) and whole-body insulin sensitivity (Matsuda index: −1.67 [−0.50, −2.84], p = 0.009). Post-glucose hyperinsulinemia (mean insulin: +99 [17, 182] pmol/L, p = 0.009) resulted from reduced insulin clearance (−0.16 [−0.32, −0.01] L min−1 m−2, p = 0.04) and enhanced hyperglycemia-induced total insulin secretion (+11.9 [1.1, 22.8] nmol/m2, p = 0.02), which occurred despite a decline in model-derived β cell glucose sensitivity (−41 [−74, −7] pmol min−1 m−2 mmol−1 L, p = 0.04). The analysis of tracer-derived glucose metabolic fluxes during lipid infusion revealed lower glucose clearance (−96 [−152, −41] mL/kgFFM, p = 0.005), increased 2-hour oral glucose absorption (+380 [42, 718] μmol/kgFFM, p = 0.04) and suppressed endogenous glucose production (−448 [−573, −123] μmol/kgFFM, p = 0.005). High-physiologic triglyceride levels increased acute basal insulin secretion in murine pseudoislets (+11 [3, 19] pg/aliquot, p = 0.02) and human pancreatic islets (+286 [59, 512] pg/islet, p = 0.02). Our findings support a critical role for hypertriglyceridemia in the pathogenesis of type 2 diabetes in otherwise healthy individuals and dissect the glucose homeostatic mechanisms involved, encompassing insulin sensitivity, β cell function and oral glucose absorption. [Display omitted] •Mild acute hypertriglyceridemia has marked negative effects on oral glucose tolerance.•Mechanisms include whole body insulin resista
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We aimed to comprehensively examine the effects of hypertriglyceridemia on major glucose homeostatic mechanisms involved in diabetes progression. In this randomized, cross-over, single-blinded study, two dual-labeled, 3-hour oral glucose tolerance tests were performed during 5-hour intravenous infusions of either 20 % Intralipid or saline in 12 healthy subjects (age 27.9 ± 2.6 years, 11 men, BMI 22.6 ± 1.4 kg/m2) to evaluate lipid-induced changes in insulin metabolism and glucose kinetics. Insulin sensitivity, β cell secretory function, and insulin clearance were assessed by modeling glucose, insulin and C-peptide data. Intestinal glucose absorption, endogenous glucose production, and glucose clearance were assessed from glucose tracers. The effect of triglycerides on β-cell secretory function was examined in perifusion experiments in murine pseudoislets and human pancreatic islets. Mild acute hypertriglyceridemia impaired oral glucose tolerance (mean glucose: +0.9 [0.3, 1.5] mmol/L, p = 0.008) and whole-body insulin sensitivity (Matsuda index: −1.67 [−0.50, −2.84], p = 0.009). Post-glucose hyperinsulinemia (mean insulin: +99 [17, 182] pmol/L, p = 0.009) resulted from reduced insulin clearance (−0.16 [−0.32, −0.01] L min−1 m−2, p = 0.04) and enhanced hyperglycemia-induced total insulin secretion (+11.9 [1.1, 22.8] nmol/m2, p = 0.02), which occurred despite a decline in model-derived β cell glucose sensitivity (−41 [−74, −7] pmol min−1 m−2 mmol−1 L, p = 0.04). The analysis of tracer-derived glucose metabolic fluxes during lipid infusion revealed lower glucose clearance (−96 [−152, −41] mL/kgFFM, p = 0.005), increased 2-hour oral glucose absorption (+380 [42, 718] μmol/kgFFM, p = 0.04) and suppressed endogenous glucose production (−448 [−573, −123] μmol/kgFFM, p = 0.005). High-physiologic triglyceride levels increased acute basal insulin secretion in murine pseudoislets (+11 [3, 19] pg/aliquot, p = 0.02) and human pancreatic islets (+286 [59, 512] pg/islet, p = 0.02). Our findings support a critical role for hypertriglyceridemia in the pathogenesis of type 2 diabetes in otherwise healthy individuals and dissect the glucose homeostatic mechanisms involved, encompassing insulin sensitivity, β cell function and oral glucose absorption. 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Mild acute hypertriglyceridemia impaired oral glucose tolerance (mean glucose: +0.9 [0.3, 1.5] mmol/L, p = 0.008) and whole-body insulin sensitivity (Matsuda index: −1.67 [−0.50, −2.84], p = 0.009). Post-glucose hyperinsulinemia (mean insulin: +99 [17, 182] pmol/L, p = 0.009) resulted from reduced insulin clearance (−0.16 [−0.32, −0.01] L min−1 m−2, p = 0.04) and enhanced hyperglycemia-induced total insulin secretion (+11.9 [1.1, 22.8] nmol/m2, p = 0.02), which occurred despite a decline in model-derived β cell glucose sensitivity (−41 [−74, −7] pmol min−1 m−2 mmol−1 L, p = 0.04). The analysis of tracer-derived glucose metabolic fluxes during lipid infusion revealed lower glucose clearance (−96 [−152, −41] mL/kgFFM, p = 0.005), increased 2-hour oral glucose absorption (+380 [42, 718] μmol/kgFFM, p = 0.04) and suppressed endogenous glucose production (−448 [−573, −123] μmol/kgFFM, p = 0.005). High-physiologic triglyceride levels increased acute basal insulin secretion in murine pseudoislets (+11 [3, 19] pg/aliquot, p = 0.02) and human pancreatic islets (+286 [59, 512] pg/islet, p = 0.02). Our findings support a critical role for hypertriglyceridemia in the pathogenesis of type 2 diabetes in otherwise healthy individuals and dissect the glucose homeostatic mechanisms involved, encompassing insulin sensitivity, β cell function and oral glucose absorption. [Display omitted] •Mild acute hypertriglyceridemia has marked negative effects on oral glucose tolerance.•Mechanisms include whole body insulin resistance and faster glucose absorption.•These effects are attenuated by lipid-induced hyperinsulinemia.</description><subject>Beta cell function</subject><subject>Fatty acids</subject><subject>Glucose absorption</subject><subject>Glucose intolerance</subject><subject>Glucose kinetics</subject><subject>Hypertriglyceridemia</subject><subject>Insulin clearance</subject><subject>Insulin resistance</subject><subject>Insulin secretion</subject><subject>Lipotoxicity</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNqFkE9LxDAQxYMouK5-BKFHL12TtGnTk8jiP1jwoueQJlN31jZdk7aw394s3YM3T_MY3hvm_Qi5ZXTFKCvud6sOBl337YpTzldMCJ6XZ2TBRMZTWVB6ThaU8iKleSUuyVUIO0ppWcpiQaYN7tGm6OxowCZf7Wj6AAm6oW_Ba2eiDon1OIFL6kOC3V6j_-P8RgcDmpBoZ2MsjC265PQPhi6uki3odtjGrLM4oR11G67JRRMH3Jzmknw-P32sX9PN-8vb-nGTmkxWQ6oba2rGTV7kTWljrYaz3BoG1mgJUfIaBK0qLjLNWdPUgnEpKyszlkFNy2xJ7ua7e9__jBAG1WEw0LbaQT8GxQvJJOOFOFrFbDW-D8FDo_YeO-0PilF15Kx26tRLHTmrmXPMPcw5iD0mBK-CQYjgbORkBmV7_OfCL1wNjAQ</recordid><startdate>202209</startdate><enddate>202209</enddate><creator>Tricò, Domenico</creator><creator>Mengozzi, Alessandro</creator><creator>Baldi, Simona</creator><creator>Bizzotto, Roberto</creator><creator>Olaniru, Oladapo</creator><creator>Toczyska, Klaudia</creator><creator>Huang, Guo Cai</creator><creator>Seghieri, Marta</creator><creator>Frascerra, Silvia</creator><creator>Amiel, Stephanie A.</creator><creator>Persaud, Shanta</creator><creator>Jones, Peter</creator><creator>Mari, Andrea</creator><creator>Natali, Andrea</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202209</creationdate><title>Lipid-induced glucose intolerance is driven by impaired glucose kinetics and insulin metabolism in healthy individuals</title><author>Tricò, Domenico ; Mengozzi, Alessandro ; Baldi, Simona ; Bizzotto, Roberto ; Olaniru, Oladapo ; Toczyska, Klaudia ; Huang, Guo Cai ; Seghieri, Marta ; Frascerra, Silvia ; Amiel, Stephanie A. ; Persaud, Shanta ; Jones, Peter ; Mari, Andrea ; Natali, Andrea</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-afdcb12c464f7d524f214dc1edca8e14d2be5099253a21ffb512889d8313eb073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Beta cell function</topic><topic>Fatty acids</topic><topic>Glucose absorption</topic><topic>Glucose intolerance</topic><topic>Glucose kinetics</topic><topic>Hypertriglyceridemia</topic><topic>Insulin clearance</topic><topic>Insulin resistance</topic><topic>Insulin secretion</topic><topic>Lipotoxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tricò, Domenico</creatorcontrib><creatorcontrib>Mengozzi, Alessandro</creatorcontrib><creatorcontrib>Baldi, Simona</creatorcontrib><creatorcontrib>Bizzotto, Roberto</creatorcontrib><creatorcontrib>Olaniru, Oladapo</creatorcontrib><creatorcontrib>Toczyska, Klaudia</creatorcontrib><creatorcontrib>Huang, Guo Cai</creatorcontrib><creatorcontrib>Seghieri, Marta</creatorcontrib><creatorcontrib>Frascerra, Silvia</creatorcontrib><creatorcontrib>Amiel, Stephanie A.</creatorcontrib><creatorcontrib>Persaud, Shanta</creatorcontrib><creatorcontrib>Jones, Peter</creatorcontrib><creatorcontrib>Mari, Andrea</creatorcontrib><creatorcontrib>Natali, Andrea</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tricò, Domenico</au><au>Mengozzi, Alessandro</au><au>Baldi, Simona</au><au>Bizzotto, Roberto</au><au>Olaniru, Oladapo</au><au>Toczyska, Klaudia</au><au>Huang, Guo Cai</au><au>Seghieri, Marta</au><au>Frascerra, Silvia</au><au>Amiel, Stephanie A.</au><au>Persaud, Shanta</au><au>Jones, Peter</au><au>Mari, Andrea</au><au>Natali, Andrea</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipid-induced glucose intolerance is driven by impaired glucose kinetics and insulin metabolism in healthy individuals</atitle><jtitle>Metabolism, clinical and experimental</jtitle><date>2022-09</date><risdate>2022</risdate><volume>134</volume><spage>155247</spage><epage>155247</epage><pages>155247-155247</pages><artnum>155247</artnum><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>Hypertriglyceridemia is associated with an increased risk of type 2 diabetes. We aimed to comprehensively examine the effects of hypertriglyceridemia on major glucose homeostatic mechanisms involved in diabetes progression. In this randomized, cross-over, single-blinded study, two dual-labeled, 3-hour oral glucose tolerance tests were performed during 5-hour intravenous infusions of either 20 % Intralipid or saline in 12 healthy subjects (age 27.9 ± 2.6 years, 11 men, BMI 22.6 ± 1.4 kg/m2) to evaluate lipid-induced changes in insulin metabolism and glucose kinetics. Insulin sensitivity, β cell secretory function, and insulin clearance were assessed by modeling glucose, insulin and C-peptide data. Intestinal glucose absorption, endogenous glucose production, and glucose clearance were assessed from glucose tracers. The effect of triglycerides on β-cell secretory function was examined in perifusion experiments in murine pseudoislets and human pancreatic islets. Mild acute hypertriglyceridemia impaired oral glucose tolerance (mean glucose: +0.9 [0.3, 1.5] mmol/L, p = 0.008) and whole-body insulin sensitivity (Matsuda index: −1.67 [−0.50, −2.84], p = 0.009). Post-glucose hyperinsulinemia (mean insulin: +99 [17, 182] pmol/L, p = 0.009) resulted from reduced insulin clearance (−0.16 [−0.32, −0.01] L min−1 m−2, p = 0.04) and enhanced hyperglycemia-induced total insulin secretion (+11.9 [1.1, 22.8] nmol/m2, p = 0.02), which occurred despite a decline in model-derived β cell glucose sensitivity (−41 [−74, −7] pmol min−1 m−2 mmol−1 L, p = 0.04). The analysis of tracer-derived glucose metabolic fluxes during lipid infusion revealed lower glucose clearance (−96 [−152, −41] mL/kgFFM, p = 0.005), increased 2-hour oral glucose absorption (+380 [42, 718] μmol/kgFFM, p = 0.04) and suppressed endogenous glucose production (−448 [−573, −123] μmol/kgFFM, p = 0.005). High-physiologic triglyceride levels increased acute basal insulin secretion in murine pseudoislets (+11 [3, 19] pg/aliquot, p = 0.02) and human pancreatic islets (+286 [59, 512] pg/islet, p = 0.02). Our findings support a critical role for hypertriglyceridemia in the pathogenesis of type 2 diabetes in otherwise healthy individuals and dissect the glucose homeostatic mechanisms involved, encompassing insulin sensitivity, β cell function and oral glucose absorption. [Display omitted] •Mild acute hypertriglyceridemia has marked negative effects on oral glucose tolerance.•Mechanisms include whole body insulin resistance and faster glucose absorption.•These effects are attenuated by lipid-induced hyperinsulinemia.</abstract><pub>Elsevier Inc</pub><doi>10.1016/j.metabol.2022.155247</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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source ScienceDirect Freedom Collection (Elsevier)
subjects Beta cell function
Fatty acids
Glucose absorption
Glucose intolerance
Glucose kinetics
Hypertriglyceridemia
Insulin clearance
Insulin resistance
Insulin secretion
Lipotoxicity
title Lipid-induced glucose intolerance is driven by impaired glucose kinetics and insulin metabolism in healthy individuals
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