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Chronic effects of different non-esterified fatty acids on pancreatic islets of rats

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Abstract

Aims: The aim of this study was to examine the chronic effects of different non-esterified fatty acids (NEFA) on insulin secretion by pancreatic islets of normal Wistar rats in vitro. Methods: Pancreatic islets were isolated from normal Wistar rats, and were incubated with 0.2, 0.4, or 0.8 mmol/L palmitate (C16:0), stearate (C18:0), oleate (C18:1), or linoleate (C18:2) for 24 h, then the insulin secretion and pyruvate dehydrogenase (PHD) activity were examined. Results: Neither islet insulin content nor islet DNA content differed among islets incubated with each kind of NEFA. Compared with control, linoleate significantly inhibited glucose-stimulated insulin secretion (GSIS) and PDH activity at each concentration (p<0.05), while others inhibited GSIS and PDH activity significantly only at 0.4 and 0.8 mmol/L (p<0.05). There was no significant difference in GSIS and PDH activity among islets pretreated by palmitate, stearate, and oleate at the same concentration (p>0.05). However, linoleate decreased GSIS more than others at the same concentration (p<0.05), while linoleate (0.4 or 0.8 mmol/L) inhibited PDH activity more than others at the same concentration (p<0.05). Conclusions: Elevation of palmitate, stearate, oleate or linoleate decreases the β-cell secretory response to glucose, through inhibiting PDH activity. Linoleate exerts more negative effect on GSIS than other NEFA.

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Authors and Affiliations

  1. Department of Endocrinology, The 4th Affiliated Hospital, HeBei Medical University, 050011, ShiJiazhuang, HeBei, China

    Yuan Wang MD

  2. Department of Health Sciences, Medical School, Peking University, Peking, China

    Pei-Yu Wang

  3. Yamanashi Health Hospital, Yamanashi, Japan

    Kaneko Takashi

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  1. Yuan Wang MD
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  2. Pei-Yu Wang
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  3. Kaneko Takashi
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Correspondence to Yuan Wang MD.

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Wang, Y., Wang, PY. & Takashi, K. Chronic effects of different non-esterified fatty acids on pancreatic islets of rats. Endocr 29, 169–173 (2006). https://doi.org/10.1385/ENDO:29:1:169

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  • DOI: https://doi.org/10.1385/ENDO:29:1:169

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