Attenuation of Diabetic Hyperphagia in Neuropeptide Y–Deficient Mice is a research paper published in Diabetes (2002). On theSindex it has a DataRank of 3.2. It has been cited 76 times, with 69 citing works in its 1-hop citation network.
The combined effects of increased hypothalamic signaling by neuropeptide Y (NPY) and decreased signaling by melanocortins are hypothesized to stimulate food intake when body fat stores are depleted. To investigate NPY’s role in the hyperphagic response to uncontrolled diabetes, streptozotocin (STZ) (200 mg/kg intraperitoneally) or saline vehicle was given to NPY-deficient (Npy–/–) and wild-type (Npy+/+) mice. In Npy+/+ mice, STZ-induced diabetes increased mean daily food intake to plateau values 50% above baseline intake (+2.0 ± 0.6 g/day; P ≤ 0.05), an effect that was not seen in STZ-treated Npy–/– mice (+0.8 ± 0.1 g/day; NS), despite comparably elevated levels of plasma glucose and comparably decreased levels of body weight, fat content, and plasma leptin. Unlike the impaired feeding response to uncontrolled diabetes, Npy–/– mice exhibit intact hyperphagic responses to fasting (Erickson et al. [1], Nature 381:415–418, 1996). To investigate whether differences in hypothalamic melanocortin signaling can explain this discrepancy, we used in situ hybridization to compare the effects of STZ-diabetes and fasting on pro-opiomelanocortin (POMC) and agouti-related peptide (AgRP) mRNA levels in the hypothalamic arcuate nucleus (ARC) of Npy–/– and Npy+/+ mice. AgRP mRNA levels were increased by both fasting and STZ-diabetes, but the increase in STZ-diabetes was small (50–80%) compared with the effect of fasting (∼20-fold increase of AgRP mRNA). STZ-diabetes also lowered POMC mRNA levels by 65% in the ARC of Npy+/+ mice (P ≤ 0.05) but by only 11% in Npy–/– mice (NS); fasting significantly lowered POMC mRNA levels in both genotypes. We conclude that NPY is required for both the increase of food intake and the decrease of hypothalamic POMC gene expression induced by uncontrolled diabetes. In contrast, NPY is not required for either of these responses when the stimulus is food deprivation. Moreover, fasting is a more potent stimulus to hypothalamic AgRP gene expression than is STZ-diabetes. Therefore, central nervous system melanocortin signaling appears to be suppressed more effectively by fasting than by uncontrolled diabetes, which provides a plausible explanation for differences in the feeding response to these two stimuli in mice lacking NPY.
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Base Score Contribution
0.652
From this paper's citation signal
Citation Network Contribution
2.6
From 62 citing papers with measurable signal
Ranked by citation count — the same ordering the engine uses when summing log1p(Cq) over citers.
DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 20% comes from its base citations and 80% from the citation network (62 citing papers contributed measurable signal).
Citers are pulled from OpenAlex sorted by cited_by_count:descand capped per paper, so when the cap binds we keep the highest-signal references and the score is reproducible across reruns.
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