Postprandial Lipemia Modulates Pancreatic Alpha-Cell Function in the Prediction of Type 2 Diabetes Development: The CORDIOPREV Study

Pozuelo-Sanchez, Isabel; Villasanta‐Gonzalez, Alejandro; Alcalá‐Díaz, Juan F.; Vals-Delgado, Cristina; León-Acuña, Ana; Gonzalez-Requero, Anabel; Yubero‐Serrano, Elena M.; Luque, Raúl M; Caballero-Villarraso, Javier; Quesada, Iván; Ordovás, José M.; Pérez‐Martínez, Pablo; Roncero-Ramos, Irene

doi:10.1021/acs.jafc.9b06801

“…Previous studies have found that T2DM is associated with abnormalities in lipid metabolism such as high fasting and postprandial blood levels of TG, high concentrations of nonesterified fatty acids, and low HDL concentrations [ 9 ]. In addition, a study has reported that hyperlipidemia can increase glucagon in patients with T2DM [ 10 ]. However, the relationship between blood lipid levels and the function of pancreatic α and β cells has been rarely studied.…”

Section: Introductionmentioning

confidence: 99%

Functional Status of Pancreatic α and β Cells in Type 2 Diabetes Mellitus Patients with Different Plasma Triglyceride Levels: A Retrospective Analysis

Guo

¹

,

Ma

²

,

Wu

³

et al. 2021

International Journal of Endocrinology

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Objective. To investigate the functional status of pancreatic α and β cells in Type 2 diabetes mellitus (T2DM) patients with different plasma triglyceride (TG) levels. TG levels can be prognostic markers for T2DM. Methods. A total of 328 patients with T2DM were divided into three groups according to different TG levels: the TGL group: TG < 1.7 mmol/L; TGM group: 1.7 mmol/L ≤ TG < 2.3 mmol/L; and TGH group: TG ≥ 2.3 mmol/L. An oral glucose tolerance test (OGTT), insulin release test, and glucagon release test were performed in each patient. The changes of glucagon, glucagon/insulin ratio, early insulin secretion index ( Δ I 30 / Δ G 30 ), and area under the insulin curve (AUCI) were compared among each group. Also, the correlations between glucagon and pancreatic β-cell function, glycosylated hemoglobin (HbA1c), and other indices were analyzed. Results. With the increase of TG, the fasting and postprandial glucagon levels, the glucagon/insulin ratio, and the area under the glucagon curve (AUCG) presented an increasing trend. The homeostasis model assessment of insulin resistance (HOMA–IR) of the TGH group was significantly increased compared to the TGL and TGM groups. In addition to the increase in TG levels, the insulin sensitivity index (ISI), homeostasis model assessment for β-cell function index (HOMA-β), Δ I 30 / Δ G 30 , and AUCI displayed a reducing trend. Glucagon was negatively correlated with Δ I 30 / Δ G 30 , high-density lipoprotein (HDL), HOMA-β, body mass index (BMI), ISI, and AUCI ( P < 0.05 ) and positively correlated with fasting blood glucose (FPG), AUCG, HOMA-IR, HbA1c, duration, TG, low-density lipoprotein (LDL), and total cholesterol (TC) ( P < 0.05 ). Conclusion. Hypertriglyceridemia aggravated the dysfunction of pancreatic α and β cells. A reasonable control of the TG level makes it easier for blood glucose to reach the standard.

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“…Therefore, accurately reflecting the problems of lipid metabolism by measuring fasting blood lipids alone is difficult. With the increasing emphasis on postprandial lipids, postprandial dyslipidemia is also considered to be an independent risk factor for type 2 diabetes mellitus and atherosclerotic disease 8 , 24 , 25 , 26 .…”

Section: Discussionmentioning

confidence: 99%

“…Postprandial lipid concentrations are superior to fasting lipids for the prediction of cardiovascular diseases. Furthermore, high postprandial lipid concentrations, especially postprandial TG (PTG) concentrations, might induce α‐cell dysfunction in individuals with cardiovascular disease 8 , leading to a rapid decrease in insulin sensitivity 9 , and thus the development of type 2 diabetes mellitus 10 . Nevertheless, the methods and criteria used to assess postprandial lipids have not been standardized.…”

Section: Introductionmentioning

confidence: 99%

Oral fat tolerance testing identifies abnormal pancreatic β‐cell function and insulin resistance in individuals with normal glucose tolerance

Liu

¹

,

Hou

²

,

Song

³

et al. 2022

J of Diabetes Invest

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Aims/Introduction: Insulin sensitivity and b-cell function are affected by lipid metabolism disorders, even before the onset of type 2 diabetes. People are in the postprandial state most of the time. Therefore, identifying postprandial hyperlipemia is important. This study aimed to assess patients with abnormalities in lipid metabolism, but with normal glucose tolerance, using oral fat tolerance testing (OFTT) to identify defects in insulin sensitivity and b-cell function. Materials and Methods: We included 248 volunteers with normal glucose tolerance who underwent OFTT. They were divided into three groups in accordance with their fasting and 4-h postprandial triglyceride (TG) concentrations. Their lipid concentrations during OFTT were compared. The disposition index (DI) was applied to estimate b-cell function, and the Matsuda insulin sensitivity index (ISI M ) was used to assess insulin sensitivity. We used multiple linear regression analysis to estimate the relationships of fasting and postprandial TG concentrations with b-cell function and insulin sensitivity . Results: The changes in TG concentrations during OFTT were more marked than those in low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol or total cholesterol concentrations. As lipid metabolism deteriorated, the ISI M and the DI gradually decreased. Multiple linear regression analysis showed that fasting and 4-h postprandial TG concentrations affected LnISI M and LnDI. Conclusions: In individuals with normal glucose tolerance, b-cell function and insulin sensitivity gradually decrease with a deterioration in the lipid profile. Not only fasting TG, but also postprandial TG concentrations are independent risk factors for impaired b-cell function and insulin resistance.

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“…The modern diet consists of three to five feeding times a day, and individuals spend a significant amount of time in a non-fasting and postprandial state, meaning the levels of CM, VLDL, and other TRLs and their remnants are enhanced, which leads a continually fluctuating level of blood lipid ( 15 ). The postprandial metabolic status can be better reflected by postprandial TG concentration, and with the combination of fasting TG concentration, the degree of exposure of total TG in the arterial wall within 24 h can be described more comprehensively and accurately ( 16 ). TG reflects the burden of remnant cholesterol (RC) and can be used as its marker.…”

Section: Postprandial Lipemia and Postprandial Hyperlipidemiamentioning

confidence: 99%

Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

Zhao

¹

,

Liu

²

,

Yang

³

et al. 2021

Front. Cardiovasc. Med.

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Postprandial lipemia plays an important role in the formation, occurrence, and development of atherosclerosis, and it is closely related to coronary heart disease and other diseases involving endothelial dysfunction, oxidative stress, inflammation, and other mechanisms. Therefore, it has become a focus area for further research. The studies on postprandial lipemia mainly include TG, TRL, VLDL, CM, and remnant cholesterol. Diurnal triglyceride patterns and postprandial hyperlipidemia are very relevant and are now insufficiently covered. The possible mechanisms between postprandial lipemia and cardiovascular disease have been reviewed in this article by referring to relevant literature in recent years. The research progress on the effects of postprandial lipemia on endothelial function, oxidative stress, and inflammation is highlighted. The intervention of postprandial lipemia is discussed. Non-medicinal intervention such as diet and exercise improves postprandial lipemia. As medicinal intervention, statin, fibrate, ezetimibe, omega-3 fatty acids, and niacin have been found to improve postprandial lipid levels. Novel medications such as pemafibrate, PCSK9, and apoCIII inhibitors have been the focus of research in recent years. Gut microbiota is closely related to lipid metabolism, and some studies have indicated that intestinal microorganisms may affect lipid metabolism as environmental factors. Whether intervention of gut microbiota can reduce postprandial lipemia, and therefore against AS, may be worthy of further study.

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Postprandial Lipemia Modulates Pancreatic Alpha-Cell Function in the Prediction of Type 2 Diabetes Development: The CORDIOPREV Study

Cited by 4 publications

References 52 publications

Functional Status of Pancreatic α and β Cells in Type 2 Diabetes Mellitus Patients with Different Plasma Triglyceride Levels: A Retrospective Analysis

Functional Status of Pancreatic α and β Cells in Type 2 Diabetes Mellitus Patients with Different Plasma Triglyceride Levels: A Retrospective Analysis

Oral fat tolerance testing identifies abnormal pancreatic β‐cell function and insulin resistance in individuals with normal glucose tolerance

Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

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