Effect of corticotropin releasing hormone and neuropeptide Y on electrophysiological activity of sympathetic nerves to interscapular brown adipose tissue

Egawa, Masato; Yoshimatsu, Hironobu; Bray, George A.

doi:10.1016/0306-4522(90)90181-3

Cited by 101 publications

(50 citation statements)

References 24 publications

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“…20,21 Repeated injection of NPY directly into the PVN over a period of several days results in sustained hyperphagia, body weight gain and a marked increase of body fat accumulation. 22 Some of NPY's anabolic effects also arise from decreased heat production in brown adipose tissue (BAT) 23,24 via inhibition of sympathetic nervous system (SNS) outflow to this thermogenic tissue. Thus, NPY promotes net energy gain by simultaneously increasing energy intake and decreasing energy expenditure.…”

Section: Neuropeptide Ymentioning

confidence: 99%

The NPY/AgRP neuron and energy homeostasis

2001

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Kennedy hypothesized nearly 50 y ago that negative feedback regulation of body fat stores involves hormones that circulate in proportion to adiposity and enter the brain, where they exert inhibitory effects on food intake and energy balance. Recent studies implicate leptin and insulin as 'adiposity signals' to the brain that promote negative energy balance in two ways: by inhibiting 'anabolic' hypothalamic neuronal circuits that stimulate food intake and promote weight gain, and by activating 'catabolic' pathways that reduce food intake and body weight. Chief among candidate 'anabolic' effector pathways is the NPY=AgRP neuron, found only in the hypothalamic arcuate nucleus. These neurons make peptides that potently stimulate food intake not only by increasing neuropeptide Y (NPY) signaling, but by reducing melanocortin signaling via the release of agoutirelated peptide (AgRP), an endogenous melanocortin 3=4 receptor antagonist. Since NPY=AgRP neurons express receptors for leptin and insulin and are inhibited by these hormones, they are activated by a decrease of leptin or insulin signaling. Fasting, uncontrolled diabetes, and genetic leptin deficiency are examples of conditions in which food intake increases via a mechanism hypothesized to involve NPY=AgRP neurons. Data are reviewed which illustrate the role of these neurons in adaptive and maladaptive states characterized by hyperphagia and weight gain.

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Section: Neuropeptide Ymentioning

confidence: 99%

The NPY/AgRP neuron and energy homeostasis

2001

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“…States of obesity, diabetes and hypercortisolemia, are also associated with abnormal glucose homeostasis, and, consequently, increased NPY (208,231). What remains to be demonstrated is that this increase in NPY, a marker of disturbed glucose homeostasis, actually contributes in a significant fashion to the associated hyperphagia, lipogenesis and body weight gain (203,(262)(263)(264)(271)(272)(273)(274)). a greater inhibition of feeding and weight gain through its receptors in the brain (1, 14).…”

Section: Adrenal Steroids and Their Receptors In Relation To Normal Bmentioning

confidence: 99%

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Tempel

Leibowitz

1994

J Neuroendocrinology

195

127

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The glucocorticoid, corticosterone (CORT), is believed to have an important function in modulating nutrient ingestion and metabolism. Recent evidence described in this review suggests that the effects of this adrenal hormone are mediated through two steroid receptor subtypes, the type I mineralocorticoid receptor and the type II glucocorticoid receptor. These receptors, which have different affinities for CORT, respond to different levels of circulating hormone. They mediate distinct effects of the steroid, which can be distinguished by the specific nutrient ingested and by the particular period of the circadian cycle.Under normal physiological conditions, the type I receptor is tonically activated, either by low basal levels of circulating CORT (0.5-2 pg%) normally available across the circadian cycle or possibly by the mineralocorticoid aldosterone. This type I activation is required for the maintenance of fat ingestion and fat deposition that occurs during most meals of the feeding cycle. In contrast, the type II receptor is phasically activated by moderate levels of CORT (2-1 0 pg%) normally reached during the circadian peak. Activation of this receptor is required for the natural surge in carbohydrate ingestion and metabolism that is essential at the onset of the active feeding cycle when the body's glycogen stores are at their nadir, and gluconeogenesis is needed to maintain blood glucose levels. This receptor is also activated during periods of increased energy requirements, such as, after exercise and food restriction, when CORT levels rise further ( > 10 pg%) and when its catabolic effects on fat and protein stores predominate to provide additional substrates for glucose homeostasis. These functions of CORT on fat and carbohydrate balance are mediated, in part, by type I and type II receptors located within the hypothalamic paraventricular nucleus, which is known to have key functions in controlling nutrient intake and metabolism, as well as circulating CORT levels. Moreover, the type II receptors within this nucleus, in addition to the arcuate nucleus, may interact positively with the peptide, neuropeptide Y, and the catecholamine, norepinephrine, both of which act to enhance natural carbohydrate feeding and CORT release at the onset of the natural feeding cycle.Thus, under normal conditions, endogenous CORT has a primary function in controlling nutrient ingestion and metabolism over the natural circadian cycle, through the coordinated action of the type I and type II steroid receptor systems. Through this action, CORT has impact on total caloric intake and body weight gain over the long term. Moreover, under conditions of obesity, diabetes and food restriction, steroid receptor function is greatly disturbed in association with chronic high circulating levels of CORT and abnormal glucose homeostasis. These disturbances in steroid action, along with dysfunction in brain neurochemical processes, very possibly contribute to the maintenance of hyperphagia and body weight gain in obese and diabetic ...

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“…Intracerebroventricular (i.c.v.) infusion of CRF elevates sympathetic outflow as measured by increased glucose (17,19), increased brown adipose tissue (BAT) thermogenesis (20), increased uncoupling protein-1 in BAT (21), elevated sympathetic nerve activity to BAT (22,23), increased catecholamines (11,24), and increased corticosterone (11,25). Additionally, i.c.v.…”

mentioning

confidence: 99%

Vital functions of corticotropin-releasing factor (CRF) pathways in maintenance and regulation of energy homeostasis

Carlin

Vale

Bale

2006

Proc. Natl. Acad. Sci. U.S.A.

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Regulation of energy homeostasis is a vital function of the CNS requiring adaptive responses to maintain and support life after stress perturbations. The mechanisms whereby these processes occur are, however, only partially understood. A major determinate of these responses is corticotropin-releasing factor (CRF). Receptors for CRF, CRFR1 and CRFR2, have been hypothesized to play distinct roles in the alterations necessary for homeostatic maintenance. The function of CRFR2, in particular, has remained elusive despite its presence in both the CNS and periphery. In this work, we have used complimentary gene deletion and pharmacological approaches to elucidate the crucial role CRFR2 plays in the regulation of regional tissue thermogenesis and adaptive physiology. Analyses of interscapular brown adipose tissue (IBAT) thermogenesis by thermal signature analysis and the concordant biochemical changes in key sympathetic components in mice deficient for CRFR2 revealed significantly elevated basal IBAT thermogenesis and prolonged adrenergic responsivity of IBAT in older mice. Measurement of metabolic rates by indirect calorimetry after chronic high-fat diet challenge and treatment with the CRFR1 antagonist NBI-27914 revealed a decreased respiratory exchange ratio of these mice that was normalized with NBI-27914. Further, as a definitive measure for physiological pathology, mice examined in a behavioral model of differential temperature selection showed a predilection for warmer external temperatures, supporting a loss of body heat in these mice. These studies provide physiological, biochemical, and behavioral evidence for the critical participation of CRF pathways in the maintenance and adaptive responses necessary for regulation of energy homeostasis. metabolic rate ͉ stress ͉ thermogenesis ͉ brown adipose tissue ͉ sympathetic nervous system R egulation of energy homeostasis is an important function of the central nervous system (CNS) requiring adaptive responses to maintain and support life. Many central factors influence this regulation and have been shown to be vital in habituation, thermogenesis, and metabolism. A major upstream determinate of these responses is corticotropin-releasing factor (CRF). CRF rapidly mobilizes the organism for responses to stressors and also stimulates the CNS to respond to environmental challenges.CRF and its family ligands including urocortin1 (Ucn1), Ucn2 (stresscopin-related peptide), and Ucn3 (stresscopin) are key regulators in maintaining homeostasis and are likely important in the larger adaptive responses involved in allostasis. This family of neuropeptides has been shown to be important in the regulation of food intake (1-6), anxiety (7-10), and stress (11-16), as well as stimulation of sympathetic outflow (11,17,18). Intracerebroventricular (i.c.v.) infusion of CRF elevates sympathetic outflow as measured by increased glucose (17, 19), increased brown adipose tissue (BAT) thermogenesis (20), increased uncoupling protein-1 in BAT (21), elevated sympathetic nerve activity to BAT (...

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Effect of corticotropin releasing hormone and neuropeptide Y on electrophysiological activity of sympathetic nerves to interscapular brown adipose tissue

Cited by 101 publications

References 24 publications

The NPY/AgRP neuron and energy homeostasis

The NPY/AgRP neuron and energy homeostasis

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Vital functions of corticotropin-releasing factor (CRF) pathways in maintenance and regulation of energy homeostasis

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