Effect of a high-fat diet on food intake and hypothalamic neuropeptide gene expression in streptozotocin diabetes.

Chavez, Mark; Seeley, Randy J.; Havel, Peter J.; Friedman, Mark I.; Matson, Claire A.; Woods, Stephen C.; Schwartz, Michael W.

doi:10.1172/jci603

Cited by 61 publications

(50 citation statements)

References 49 publications

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“…In contrast to AgRP, we found that NPY, POMC and CRH were not affected by 35 days of HF diet in the present study. These results are inconsistent with studies in mammals which showed that NPY, POMC and CRH levels were affected by a HF diet (Guan et al, 1998;Chavez et al, 1998;Lin et al, 2000;Lukaszewski et al, 2013), implying a genetic bluntness in the response to dietary fat in avian species.…”

Section: Involvement Of Agrp In the Hf-induced Decrease In Food Intakecontrasting

confidence: 58%

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Wang

Liu

et al. 2016

Journal of Experimental Biology

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Dietary fat affects appetite and appetite-related peptides in birds and mammals; however, the effect of dietary fat on appetite is still unclear in chickens faced with different energy statuses. Two experiments were conducted to investigate the effects of dietary fat on food intake and hypothalamic neuropeptides in chickens subjected to two feeding states or two diets. In Experiment 1, chickens were fed a high-fat (HF) or low-fat (LF) diet for 35 days, and then subjected to fed (HF-fed, LF-fed) or fasted (HF-fasted, LF-fasted) conditions for 24 h. In Experiment 2, chickens that were fed a HF or LF diet for 35 days were fasted for 24 h and then re-fed with HF (HF-RHF, LF-RHF) or LF (HF-RLF, LF-RLF) diet for 3 h. The results showed that chickens fed a HF diet for 35 days had increased body fat deposition despite decreasing food intake even when the diet was altered during the re-feeding period (P<0.05). LF diet (35 days) promoted agouti-related peptide (AgRP) expression compared with HF diet (P<0.05) under both fed and fasted conditions. LF-RHF chickens had lower neuropeptide Y (NPY) expression compared with LF-RLF chickens; conversely, HF-RHF chickens had higher NPY expression than HF-RLF chickens (P<0.05). These results demonstrate: (1) that HF diet decreases food intake even when the subsequent diet is altered; (2) the orexigenic effect of hypothalamic AgRP; and (3) that dietary fat alters the response of hypothalamic NPY to subsequent energy intake. These findings provide a novel view of the metabolic perturbations associated with long-term dietary fat over-ingestion in chickens.

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Section: Involvement Of Agrp In the Hf-induced Decrease In Food Intakecontrasting

confidence: 58%

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Wang

Liu

et al. 2016

Journal of Experimental Biology

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“…This difference could be due to a higher intake of energy from the high-carbohydrate diet than that from the high-fat diet. Such an effect has been documented in other studies in diabetic rats (19). The present effect of a high-fat diet on blood glucose is, however, different from that obtained in diabetes models with a positive energy balance and obesity, such as the diabetic Zucker fa/fa rat (7,9).…”

Section: Discussioncontrasting

confidence: 46%

Influence of a high-fat diet during chronic hyperglycemia on beta-cell function in pancreatic islet transplants to streptozotocin-diabetic rats

Hiramatsu

Grill

2001

European Journal of Endocrinology

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Chronically elevated non-esterified fatty acids (NEFAs) can exert negative effects on b-cell function both in vitro and in vivo. Negative effects of fatty acids have been difficult to evaluate in overt diabetes because of the attendant hyperglycemia that gives rise to the confounding influence of`glucotoxicity'.In this work, we tested for the effects of NEFAs in diabetes by (i) taking into account potential effects of prevailing levels of hyperglycemia, and (ii) focusing on lingering (and therefore possibly more serious) effects. A diabetic transplantation model was used in which two islet grafts with 200 and 20 rat islets respectively were transplanted under the kidney capsule of syngeneic recipients previously made diabetic by streptozotocin injection. Rats were then fed either a high-fat or a low-fat diet for 7 weeks, followed by 1 week of normal laboratory chow. During dietary intervention, food was consumed ad libitum in one protocol, but was restricted in the low-fat group in a second protocol (in order to match blood-glucose levels). A high-fat diet did not affect body weight. At the end of the protocols, graftbearing kidneys were isolated and perfused. Insulin responses to 27.8 mM glucose in perfusion were uniformly absent, in keeping with previously documented effects of chronic hyperglycemia. In contrast, 10 mM arginine induced a marked increase in insulin secretion after a low-fat diet, an effect that was significantly reduced after a high-fat diet (109^39 vs 13^15 fmolamin P , 0X05 and 95^18 vs 32^5 fmolamin P , 0X05 in the 2 protocols respectively). Regardless of protocol, no effect of diet could be detected on graft contents of insulin or preproinsulin mRNA. Thus, under conditions in which influences of chronic hyperglycemia could be accounted for, a previous high-fat diet with elevated NEFAs inhibited arginine-induced insulin secretion; however, the results indicate that insulin biosynthesis and/or b-cell mass were not affected.

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“…Although there are plenty of calories in circulation, glucose is not available for oxidation. If diabetic rats are fed diets rich in fatty acids, an oxidizable fuel for diabetics, their hyperphagia subsides (32,72,76), estrous behavior is increased (4), and some measure of fertility may be restored (133).…”

Section: Calories Must Be Available For Oxidationmentioning

confidence: 99%

Neuroendocrinology of nutritional infertility

Wade¹,

Jones²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

229

166

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Natural selection has linked the physiological controls of energy balance and fertility such that reproduction is deferred during lean times, particularly in female mammals. In this way, an energetically costly process is confined to periods when sufficient food is available to support pregnancy and lactation. Even in the face of abundance, nutritional infertility ensues if energy intake fails to keep pace with expenditure. A working hypothesis is proposed in which any activity or condition that limits the availability of oxidizable fuels (e.g., undereating, excessive energy expenditure, diabetes mellitus) can inhibit both gonadotropin-releasing hormone (GnRH)/luteinizing hormone secretion and female copulatory behaviors. Decreases in metabolic fuel availability appear to be detected by cells in the caudal hindbrain. Hindbrain neurons producing neuropeptide Y (NPY) and catecholamines (CA) then project to the forebrain where they contact GnRH neurons both directly and also indirectly via corticotropin-releasing hormone (CRH) neurons to inhibit GnRH secretion. In the case of estrous behavior, the best available evidence suggests that the inhibitory NPY/CA system acts primarily via CRH or urocortin projections to various forebrain loci that control sexual receptivity. Disruption of these signaling processes allows normal reproduction to proceed in the face of energetic deficits, indicating that the circuitry responds to energy deficits and that no signal is necessary to indicate that there is an adequate energy supply. While there is a large body of evidence to support this hypothesis, the data do not exclude nutritional inhibition of reproduction by other pathways and processes, and the full story will undoubtedly be more complex than this. luteinizing hormone; estrous behavior; corticotropin-releasing hormone; neuropeptide Y; hindbrain OF NECESSITY, the physiological controls of reproduction and energy balance are closely intertwined. Living creatures require a steady stream of oxidizable substrates to fuel their many energy-consuming activities, including reproduction. But in nature, energetic demands and opportunities for meal taking can be erratic and sometimes unpredictable, necessitating the existence of physiological and behavioral strategies to maximize chances of individual survival and permit propagation of the species (21,22,200,208).A need to eat constantly is obviated by the presence of internal caloric buffers that store glycogen and fatty acids and provide sustenance in between meals and during brief fasts. When food is abundant, animals adjust their intakes to meet all demands and keep their storage depots full (or overfull in an increasing number of cases). However, a more likely scenario in nature and during human evolution is that food can be scarce or have a very high acquisition cost. In that case, animals adjust their energetic priorities, i.e., how they partition and use the available metabolic fuels (Fig.

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Effect of a high-fat diet on food intake and hypothalamic neuropeptide gene expression in streptozotocin diabetes.

Cited by 61 publications

References 49 publications

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Influence of a high-fat diet during chronic hyperglycemia on beta-cell function in pancreatic islet transplants to streptozotocin-diabetic rats

Neuroendocrinology of nutritional infertility

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