Fatty acids and insulin secretion

Amery, Caroline M.; Nattrass, M.

doi:10.1046/j.1463-1326.2000.00059.x

Cited by 14 publications

(8 citation statements)

References 57 publications

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“…Since fatty acid delivery is a major rate‐limiting factor for hepatic VLDL synthesis, elevated concentrations may contribute to hypertri‐glyceridaemia in patients with type 2 diabetes[6]. There is conflicting data on whether NEFA impair endogenous insulin secretion in humans, duration of exposure emerging as an important factor[32,33].…”

Section: Insulin Resistancementioning

confidence: 99%

Insulin resistance and β‐cell dysfunction as therapeutic targets in type 2 diabetes

Evans

Krentz

2001

Diabetes Obesity Metabolism

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Section: Insulin Resistancementioning

confidence: 99%

Insulin resistance and β‐cell dysfunction as therapeutic targets in type 2 diabetes

Evans

Krentz

2001

Diabetes Obesity Metabolism

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“…Prolonged exposure to high concentrations of palmitate has detrimental effects on β-cell viability and function [ 14 , 15 , 16 , 17 , 18 ], possibly mediated by endoplasmic reticulum stress [ 19 ], increased ROS [ 20 , 21 ], impaired mitochondrial functions [ 22 , 23 ], altered acetylation of multiple proteins [ 24 ]. We have previously shown that long-term exposure to high lipid concentrations (lipotoxicity) causes a series of alteration in pancreatic islets including relatively elevated glucagon secretion, decreased insulin secretion, loss of α-cell sensitivity to glucose, and an accumulation of triglycerides [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

The Dynamic Effects of Isosteviol on Insulin Secretion and Its Inability to Counteract the Impaired β-Cell Function during Gluco-, Lipo-, and Aminoacidotoxicity: Studies In Vitro

Rebsdorf

Hermansen

et al. 2018

Nutrients

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Isosteviol (ISV), a diterpene molecule, is an isomer of the backbone structure of a group of substances with proven antidiabetic capabilities. The aim of this study was to investigate if ISV elicits dynamic insulin release from pancreatic islets and concomitantly is able to ameliorate gluco-, lipo-, and aminoacidotoxicity in clonal β-cell line (INS-1E) in relation to cell viability and insulin secretion. Isolated mice islets placed into perifusion chambers were perifused with 3.3 mM and 16.7 mM glucose with/without 10−7 M ISV. INS-1E cells were incubated for 72 h with either 30 mM glucose, 1 mM palmitate or 10 mM leucine with or without 10−7 M ISV. Cell viability was evaluated with a Cytotoxic Fluoro-test and insulin secretion was measured in Krebs-Ringer Buffer at 3.3 mM and 16.7 mM glucose. In the presence of 3.3 mM glucose, 10−7 M ISV did not change basal insulin secretion from perifused islets. However, at a high glucose level of 16.7 mM, 10−7 M ISV elicited a 2.5-fold increase (−ISV: 109.92 ± 18.64 ng/mL vs. +ISV: 280.15 ± 34.97 ng/mL; p < 0.01). After 72 h gluco-, lipo-, or aminoacidotoxicity in INS-1E cells, ISV treatment did not significantly affect cell viability (glucotoxicity, −ISV: 19.23 ± 0.83%, +ISV: 18.41 ± 0.90%; lipotoxicity, −ISV: 70.46 ± 3.15%, +ISV: 65.38 ± 2.81%; aminoacidotoxicity: −ISV: 8.12 ± 0.63%; +ISV: 7.75 ± 0.38%, all nonsignificant). ISV did not improve impaired insulin secretion (glucotoxicity, −ISV: 52.22 ± 2.90 ng/mL, +ISV: 47.24 ± 3.61 ng/mL; lipotoxicity, −ISV: 19.94 ± 4.10 ng/mL, +ISV: 22.12 ± 3.94 ng/mL; aminoacidotoxicity: −ISV: 32.13 ± 1.00 ng/mL; +ISV: 30.61 ± 1.54 ng/mL, all nonsignificant). In conclusion, ISV acutely stimulates insulin secretion at high but not at low glucose concentrations. However, ISV did not counteract cell viability or cell dysfunction during gluco-, lipo-, or aminoacidotoxicity in INS-1E cells.

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“…Insulin secretion and insulin sensitivity increased parallel. These changes during prolonged fasting can be explained by re-esterification of NEFA to TG [25], a supposed stimulation of insulin secretion by increasing NEFA [2,[25][26][27], a down-regulated activity of the LPL and an up-regulation of the hepatic LDL receptor due to increasing insulin levels. The hypothesis that increasing NEFA caused an increase in insulin secretion is supported by an analysis of individual courses ( fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of One Week Juice Fasting on Lipid Metabolism: A Cohort Study in Healthy Subjects

Huber¹,

Nauck²,

Lüdtke³

et al. 2003

Complement Med Res

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Objective: We investigated the effects of a popular modified juice fasting program on lipid metabolism. Volunteers and Methods: 5 healthy, nonobese, male volunteers fasted for 8 days. Daily energy intake was limited to 150–300 kcal/d solely as carbohydrates (vegetable and fruit drinks). Physical activity was maintained as before. At baseline, on days 2, 3, and 8 during fasting, and on days 2 and 8 after fasting, serum lipids, lipoproteins, and insulin were investigated. Results: Juice fasting resulted in bi-phasic changes: Until day 2 and 3 triacylglycerols (TG), very low-density lipoprotein apolipoprotein B (VLDL apo B), and insulin decreased by 52, 51, and 65% respectively, while nonesterified fatty acids (NEFA), low-density lipoprotein (LDL) apo B, and LDL cholesterol increased by 363, 38, and 35%. Between day 3 and 8 NEFA increased; TG and insulin increased as well, but remained below baseline values, and LDL cholesterol normalized. After 8 days juice fasting significant changes (p < 0.05) compared to the baseline were found only for free cholesterol (-10%), phospholipids (-14%), apo AI (-9%), apo AII (-11%), insulin (-42%), C-peptide (-57%), and NEFA (+535%, p = 0.0001). Total cholesterol decreased by 9% (n.s.) after 8 days. One week after the ending of fasting all parameters returned to normal. Conclusion: Contrary to total fasting and fasting with limited physical activity, 8 days juice fasting without limitation of physical activity results in a decrease of free cholesterol and an only initial increase of LDL cholesterol. After 8 days insulin, TG, and VLDL are still lower than at baseline, however, they have increased compared to the initial phase, probably counterregulatory to a further increase of NEFA.

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Fatty acids and insulin secretion

Cited by 14 publications

References 57 publications

Insulin resistance and β‐cell dysfunction as therapeutic targets in type 2 diabetes

Insulin resistance and β‐cell dysfunction as therapeutic targets in type 2 diabetes

The Dynamic Effects of Isosteviol on Insulin Secretion and Its Inability to Counteract the Impaired β-Cell Function during Gluco-, Lipo-, and Aminoacidotoxicity: Studies In Vitro

Effects of One Week Juice Fasting on Lipid Metabolism: A Cohort Study in Healthy Subjects

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