Effects of a High‐Fat Diet and Strain on Hypothalamic Gene Expression in Rats
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Abstract Objective: This study was designed to investigate whether dietary fat and genetic background might differentially alter the expression of hypothalamic genes involved in food intake. Research Methods and Procedures: Three‐month‐old Osborne‐Mendel (OM) and S5B/Pl rats were fed either a high‐fat or a low‐fat diet for 14 days. mRNA for neuropeptide Y (NPY), corticotrophin‐releasing hormone, NPY Y‐1 receptor and Y‐5 receptor, and serotonin 2c (5‐HT2c) receptors were measured using Northern blotting or ribonuclease protection assays. Results: OM rats showed an increased expression of NPY and corticotrophin‐releasing hormone compared with S5B/Pl rats. The expression of NPY‐Y1 and ‐Y5 receptor mRNA was significantly higher in the hypothalamus of OM rats compared with S5B/Pl rats. The expression of 5HT‐2c receptor mRNA was significantly reduced in both strains of rats eating a high‐fat diet when compared with the animals eating the low‐fat diet. Discussion: These data suggest that over activity of the NPY system may contribute to the development of obesity in OM rats and that expression of the 5HT‐2c receptor gene may be modulated by dietary fat.The neuropeptide BW receptor 1 (NPBW1, provisional nomenclature [6]) is activated by two 23-amino-acid peptides, neuropeptide W (neuropeptide W-23) and neuropeptide B (neuropeptide B-23) [22, 7]. C-terminally extended forms of the peptides (neuropeptide W-30 and neuropeptide B-29) also activate NPBW1 [2]. Unique to both forms of neuropeptide B is the N-terminal bromination of the first tryptophan residue, and it is from this post-translational modification that the nomenclature NPB is derived. These peptides were first identified from bovine hypothalamus and therefore are classed as neuropeptides. Endogenous variants of the peptides without the N-terminal bromination, des-Br-neuropeptide B-23 and des-Br-neuropeptide B-29, were not found to be major components of bovine hypothalamic tissue extracts. The NPBW2 receptor is activated by the short and C-terminal extended forms of neuropeptide W and neuropeptide B [2].
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Since the discovery of neuropeptide Y which is co‐stored and co‐operate with noradrenaline (NA) in sympathetic nerve fibers, several scientific groups have searched for structures with neuropeptide Y antagonistic properties. Research has mainly focused on various peptide fragments which originate from or are related to the neuropeptide Y sequence. Some non‐peptide antagonists have been proposed but they are mostly of low potency and non‐selective. Our recent observations that α‐trinositol (D‐myo‐inositol 1.2.6‐trisphosphate) is an inhibitor of neuropeptide Y effects will hopefully lead to the development of useful non‐peptide neuropeptide Y inhibitors. As a novel approach the highly selective approach of down‐regulating neuropeptide Y receptors with antisense oligodeoxynucleotides is also discussed. Neuropeptide Y antagonistic agents would help us to understand the physiological role of neuropeptide Y and may serve as useful medication in circulation disorders.
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Neuropeptide Y (NPY ) 是为喂的有势力 neurotransmitter。也除 NPY，象刺鼠相关的蛋白质(AgRP ) 那样的开胃 neuropeptides，和象刺激荷尔蒙(MSH ) 和 cocaine-amphetamine-regulated 抄本(大车) 的 alpha-melatonin 那样的使食欲不振 neuropeptides 以外涉及中央喂规定。在禁食期间， NPY 和 AgRP 基因表情是起来调整的， POMC 和大车基因表情在视下丘是下面调整的。基于 peptidergic 神经原的网络，前者涉及积极的喂规定，和后者涉及否定的喂，它特别在帕拉施加这些喂养, 饲, 哺调整肽室的原子核(PVN ) 。在喂上澄清 NPY 系统的大美人的补偿机制，在胃口相关的 neuropeptides 和喂的行为的基因表情的变化在 NPY Y5 击倒老鼠被学习。食物摄取在 Y5 击倒老鼠被增加。禁食更深刻地在 KO 老鼠增加了食物和水吸入的数量。这些数据显示了在 Y5 击倒鼠标喂行为的补偿现象。RT-PCR 和 ISH 建议喂的赔偿在视下丘由于在 AgRP，大车和 POMC 的基因表情的变化。因此，这些调查结果显示补偿机制在弓形的原子核(弧) 在 POMC/CART 基因表示包含变化。POMC/CART 基因表示为在喂行为的中央补偿规定是重要的。
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Pancreatic polypeptide
Peptide YY
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Peptide YY
Orexigenic
Radioligand
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