Role of leptin in energy expenditure: the hypothalamic perspective

The adipocyte-derived hormone leptin is a peripheral signal that informs the brain about the metabolic status of an organism. Although traditionally viewed as an appetite-suppressing hormone, studies in the past decade have highlighted the role of leptin in energy expenditure. Leptin has been shown to increase energy expenditure in particular through its effects on the cardiovascular system and brown adipose tissue (BAT) thermogenesis via the hypothalamus. The current review summarizes the role of leptin signaling in various hypothalamic nuclei and its effects on the sympathetic nervous system to influence blood pressure, heart rate, and BAT thermogenesis. Specifically, the role of leptin signaling on three different hypothalamic nuclei, the dorsomedial hypothalamus, the ventromedial hypothalamus, and the arcuate nucleus, is reviewed. It is known that all of these brain regions influence the sympathetic nervous system activity and thereby regulate BAT thermogenesis and the cardiovascular system. Thus the current work focuses on how leptin signaling in specific neuronal populations within these hypothalamic nuclei influences certain aspects of energy expenditure.

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Impairment of trophic response of brown fat to cold in guanethidine-treated rats

AJP Cell Physiology ◽

10.1152/ajpcell.1982.242.3.c159 ◽

1982 ◽

Vol 242 (3) ◽

pp. C159-C165 ◽

Cited By ~ 38

Author(s):

G. Mory ◽

D. Ricquier ◽

M. Nechad ◽

P. Hemon

Keyword(s):

Nervous System ◽

Sympathetic Nervous System ◽

Protein A ◽

Chronic Administration ◽

Phospholipid Content ◽

Noradrenaline Content ◽

Brown Adipose ◽

Sympathetic Nervous ◽

Binding To Mitochondria

The aim of the present study was to investigate the role of the sympathetic nervous system in the trophic response of brown adipose tissue (BAT) to chronic cold exposure. The hyperplasia and the development of the mitochondria characterizing this response are usually considered as mainly controlled by the sympathetic activity in BAT, but this has never been clearly demonstrated. In the present work rats were sympathectomized by chronic administration of guanethidine and then exposed to cold during two weeks. The treatment induced a strong reduction of the noradrenaline content of BAT. The trophic response of the tissue to cold was largely impaired: no increase of the tissue weight, weak increase in the DNA, protein, and phospholipid content of the tissue. The development of the mitochondria was almost abolished. The increase in the proportion of the 32,000-dalton protein, a protein which regulates heat production by BAT, was suppressed and the GDP-binding to mitochondria, which is an index of BAT thermogenic capacity, was not increased as in normal cold-adapted rats. The ultrastructure of the tissue remained the same as in warm-adapted animals. It is concluded that the sympathetic nervous system plays an essential role in the control of the trophic response of BAT to the cold.

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The role of the vegetative part of sympathetic nervous system in development of cardiovascular complications in patients with arterial hypertension: pharmacological aspects

Systemic Hypertension ◽

10.26442/sg29059 ◽

2014 ◽

Vol 11 (3) ◽

pp. 88-94

Author(s):

S R Gilyarevsky

Keyword(s):

Nervous System ◽

Sympathetic Nervous System ◽

Arterial Hypertension ◽

Cardiovascular System ◽

Antihypertensive Agents ◽

Cardiovascular Complications ◽

Autonomic Regulation ◽

Sympathetic Nervous ◽

The Impact

Recently, we have determined new interest in studying the role of sympathetic part of autonomic division of nervous system (SANS) in the pathogenesis of arterial hypertension (AH), as well as in studying the role of agents, suppressing the activity of SANS, using for AH treatment, including the usage of antihypertensive agents and non-pharmacological methods. This article discusses the changes of autonomic regulation of the cardiovascular system in patients with AH. The role of these changes in the development of the functional and structured changes of the heart and systemic vessels can be observing during long-standing AH and will lead to the development of adverse clinical outcomes. We have been showing received data, associated with the impact of non-medicated and pharmacological approaches to the autonomic regulation of the cardiovascular system.

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Insulin and the Regulation of the Cardiovascular System: Role of the l-arginine Nitric Oxide Pathway and the Sympathetic Nervous System

The Endothelium in Cardiovascular Disease ◽

10.1007/978-3-642-79803-0_10 ◽

1995 ◽

pp. 108-128 ◽

Cited By ~ 2

Author(s):

U. Scherrer

Keyword(s):

Nitric Oxide ◽

Nervous System ◽

Sympathetic Nervous System ◽

Cardiovascular System ◽

Sympathetic Nervous ◽

Nitric Oxide Pathway

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Role of sympathetic nervous system in immobilization- and cold-induced brown adipose tissue thermogenesis in rats.

The Japanese Journal of Physiology ◽

10.2170/jjphysiol.34.103 ◽

1984 ◽

Vol 34 (1) ◽

pp. 103-111 ◽

Cited By ~ 26

Author(s):

Hiroyuki SHIBATA ◽

Tetsuo NAGASAKA

Keyword(s):

Nervous System ◽

Adipose Tissue ◽

Sympathetic Nervous System ◽

Brown Adipose Tissue ◽

Brown Adipose ◽

Brown Adipose Tissue Thermogenesis ◽

Sympathetic Nervous

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Involvement of sympathetic nervous system and brown fat in endotoxin-induced fever in rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.255.5.e617 ◽

1988 ◽

Vol 255 (5) ◽

pp. E617-E620 ◽

Cited By ~ 5

Author(s):

M. M. Jepson ◽

D. J. Millward ◽

N. J. Rothwell ◽

M. J. Stock

Keyword(s):

Nervous System ◽

Sympathetic Nervous System ◽

Beta Adrenoceptor ◽

Adrenoceptor Antagonist ◽

Brown Adipose ◽

Sympathetic Nervous ◽

Escherichia Coli Lipopolysaccharide ◽

Marked Suppression

The object of this study was to assess the role of brown adipose tissue (BAT) and the sympathetic nervous system in the rise in heat production associated with endotoxin-induced fever. Oxygen consumption (VO2) was found to be significantly increased (28%) over a 4-h period after two doses of endotoxin (Escherichia coli lipopolysaccharide, 0.3 mg/100 g body wt) given 24 h apart. Injection of a mixed beta-adrenoceptor antagonist (propranolol) reduced VO2 by 14% in endotoxin-treated rats, whereas the selective beta 1- (atenolol) or beta 2- (ICI 118551) antagonists suppressed VO2 by 10%. These drugs did not affect VO2 in control animals. BAT thermogenic activity assessed from measurements of in vitro mitochondrial guanosine 5'-diphosphate (GDP) binding was elevated by 54% in interscapular BAT and by 171% in other BAT depots. Surgical denervation of one lobe of the interscapular depot prevented these responses. Endotoxin failed to stimulate GDP binding in rats fed protein-deficient diets. This may have been because BAT thermogenic activity was already elevated in control rats fed these diets or because endotoxin caused a marked suppression of food intake in the protein-deficient animals. The results indicate that sympathetic activation of BAT is involved in the thermogenic responses to endotoxin and that these can be modified by dietary manipulation.

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Thyroid hormone-catecholamine interrelationships during exposure to cold

Acta Endocrinologica ◽

10.1530/acta.0.0970091 ◽

1981 ◽

Vol 97 (1) ◽

pp. 91-97 ◽

Cited By ~ 21

Author(s):

H. Storm ◽

C. van Hardeveld ◽

A. A. H. Kassenaar

Keyword(s):

Nervous System ◽

Plasma Concentration ◽

Thyroid Hormone ◽

Sympathetic Nervous System ◽

Plasma Levels ◽

Surgical Procedure ◽

Exposure To Cold ◽

Basal Plasma ◽

Sympathetic Nervous

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.

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