scholarly journals Brain–adipose tissue cross talk

2005 ◽  
Vol 64 (1) ◽  
pp. 53-64 ◽  
Author(s):  
Timothy J. Bartness ◽  
C. Kay Song ◽  
Haifei Shi ◽  
Robert R. Bowers ◽  
Michelle T. Foster
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Body Fat ◽  
Pseudorabies Virus ◽  
Sensory Nerve ◽  
Sensory Innervation ◽  
Electrophysiological Recording ◽  
Surgical Removal ◽  
Fat Cell ◽  
The Brain

While investigating the reversible seasonal obesity of Siberian hamsters, direct sympathetic nervous system (SNS) postganglionic innervation of white adipose tissue (WAT) has been demonstrated using anterograde and retrograde tract tracers. The primary function of this innervation is lipid mobilization. The brain SNS outflow to WAT has been defined using the pseudorabies virus (PRV), a retrograde transneuronal tract tracer. These PRV-labelled SNS outflow neurons are extensively co-localized with melanocortin-4 receptor mRNA, which, combined with functional data, suggests their involvement in lipolysis. The SNS innervation of WAT also regulates fat cell number, as noradrenaline inhibits and WAT denervation stimulates fat cell proliferation in vitro and in vivo respectively. The sensory innervation of WAT has been demonstrated by retrograde tract tracing, electrophysiological recording and labelling of the sensory-associated neuropeptide calcitonin gene-related peptide in WAT. Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by non-excised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey information about body fat levels to the brain. Finally, parasympathetic nervous system innervation of WAT has been suggested, but the recent finding of no WAT immunoreactivity for the possible parasympathetic marker vesicular acetylcholine transporter (VAChT) argues against this claim. Collectively, these data suggest several roles for efferent and afferent neural innervation of WAT in body fat regulation.

White adipose tissue sensory nerve denervation mimics lipectomy-induced compensatory increases in adiposity

2005 ◽  
Vol 289 (2) ◽  
pp. R514-R520 ◽  
Author(s):  
Haifei Shi ◽  
Timothy J. Bartness
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
White Adipose Tissue ◽  
Sensory Nerve ◽  
Sensory Innervation ◽  
Siberian Hamsters ◽  
Total Body Fat ◽  
Total Body ◽  
Lipid Stores ◽  
The Brain

The sensory innervation of white adipose tissue (WAT) is indicated by the labeling of sensory bipolar neurons in the dorsal root ganglion after retrograde dye placement into WAT. In addition, immunoreactivity (ir) for sensory-associated neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P in WAT pads also supports the notion of WAT sensory innervation. The function of this sensory innervation is unknown but could involve conveying the degree of adiposity to the brain. In tests of total body fat regulation, partial surgical lipectomy triggers compensatory increases in the mass of nonexcised WAT, ultimately resulting in restoration of total body fat levels in Siberian hamsters and other animals. The signal that triggers this compensation is unknown but could involve disruption of WAT sensory innervation that accompanies lipectomy. Therefore, a local and selective sensory denervation was accomplished by microinjecting the sensory nerve neurotoxin capsaicin bilaterally into epididymal WAT (EWAT) of Siberian hamsters, whereas controls received vehicle injections. Additional hamsters had bilateral EWAT lipectomy (EWATx) or sham lipectomy. As seen previously, EWATx resulted in significantly increased retroperitoneal WAT (RWAT) and inguinal WAT (IWAT) masses. Capsaicin treatment significantly decreased CGRP- but not tyrosine hydroxylase-ir, attesting to the diminished and selective sensory innervation. Capsaicin-treated hamsters also had increased RWAT and, to a lesser degree, IWAT mass largely mimicking the WAT mass increases seen after lipectomy. Collectively, these data suggest the possibility that information related to peripheral lipid stores may be conveyed to the brain via the sensory innervation of WAT.

Innervation of mammalian white adipose tissue: implications for the regulation of total body fat

1998 ◽  
Vol 275 (5) ◽  
pp. R1399-R1411 ◽  
Author(s):  
Timothy J. Bartness ◽  
Maryam Bamshad
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Body Fat ◽  
White Adipose Tissue ◽  
Regional Differences ◽  
Sensory Innervation ◽  
Exact Nature ◽  
Total Body Fat ◽  
The Central Nervous System ◽  
Total Body

We review the extensive physiological and neuroanatomical evidence for the innervation of white adipose tissue (WAT) by the sympathetic nervous system (SNS) as well as what is known about the sensory innervation of this tissue. The SNS innervation of WAT appears to be a part of the general SNS outflow from the central nervous system, consisting of structures and connections throughout the neural axis. The innervation of WAT by the SNS could play a role in the regulation of total body fat in general, most likely plays an important role in regional differences in lipid mobilization specifically, and may have a trophic affect on WAT. The exact nature of the SNS innervation of WAT is not known but it may involve contact with adipocytes and/or their associated vasculature. We hypothesize that the SNS innervation of WAT is an important contributor to the apparent “regulation” of total body fat.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.

scholarly journals Influence of feeding level and of protein level in early life on the cellularity of adipose tissue and body fat content of growing pigs

1983 ◽  
Vol 49 (1) ◽  
pp. 109-118 ◽  
Author(s):  
R. G. Campbell ◽  
A. C. Dunkin
Keyword(s):  
Adipose Tissue ◽  
Cell Size ◽  
Body Fat ◽  
Subcutaneous Adipose Tissue ◽  
Fat Content ◽  
Fat Cell ◽  
Fat Cell Size ◽  
Body Fat Content ◽  
Dry Diet ◽  
Subcutaneous Adipose

1. The effects of level of feeding and level of protein in the early postnatal period on the cellularity of subcutaneous adipose tissue and body fat content of pigs were investigated in two experiments.2. In Expt 1, piglets were given a common liquid diet at energy intakes equivalent to 2·8 or 5·2 times energy for maintenance (M) between 1·8 and 6·5 kg live weight (LW), and a common dry diet at 2·8 or 4·5 M between 6·5 and 20 kg LW. Between 20 and 75 kg LW all pigs were given a second dry diet at 4·0 M.3. In both experiments the effects of nutritional treatments on fat cell number at 20 and 75 kg LW (Expt 1) and at 45 kg LW (Expt 2) were assessed by measuring the DNA content of the subcutaneous adipose tissue contained in the left shoulder joint. Fat cell size was assessed in the same tissue by measuring the diameter of collagenase-released adipocytes.4. In Expt 1, raising the level of feeding between 1·8 and 6·5 kg LW increased body fat content and average fat cell diameter at both 6·5 (P < 0·01) and 20 kg LW (P < 0·05) but had no effect on either measurement at 75 kg LW. Similarly, raising the level of feeding between 6·5 and 20 kg LW increased body fat content and fat cell size at both 20 (P < 0·01) and 75 kg LW (P < 0·05). There was an almost twofold increase in the DNA content of subcutaneous adipose tisuue between 20 and 75 kg LW. However, it was not significantly affected at either weight by level of feeding before or subsequent to 6·5 kg LW.5. In Expt 2, reducing the level of dietary protein between 1·8 and 6·5 kg LW increased body fat content (P < 0·01) and fat cell size (P < 0·01) at the latter weight. Although level of dietary protein to 6·5 kg LW had no effect on body fat content or the weight of subcutaneous adipose tissue in the shoulder joint at 45 kg LW, pigs given the lowest-protein diet contained less DNA (P < 0·05) in the subcutaneous adipose tissue and had larger (P < 0·05) fat cells than those given the highest-protein diet to 6·5 kg LW. Reducing the protein content of the diet fed subsequent to 6·5 kg LW increased the body fat content (P < 0·01) and fat cell size (P < 0·01) at 45 kg LW.

scholarly journals Central Fibroblast Growth Factor 21 Browns White Fat via Sympathetic Action in Male Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (7) ◽  
pp. 2470-2481 ◽  
Author(s):  
Nicholas Douris ◽  
Darko M. Stevanovic ◽  
ffolliott M. Fisher ◽  
Theodore I. Cisu ◽  
Melissa J. Chee ◽  
...  
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Sympathetic Nervous System ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Male Mice ◽  
Sympathetic Nervous ◽  
The Brain

Fibroblast growth factor 21 (FGF21) has multiple metabolic actions, including the induction of browning in white adipose tissue. Although FGF21 stimulated browning results from a direct interaction between FGF21 and the adipocyte, browning is typically associated with activation of the sympathetic nervous system through cold exposure. We tested the hypothesis that FGF21 can act via the brain, to increase sympathetic activity and induce browning, independent of cell-autonomous actions. We administered FGF21 into the central nervous system via lateral ventricle infusion into male mice and found that the central treatment increased norepinephrine turnover in target tissues that include the inguinal white adipose tissue and brown adipose tissue. Central FGF21 stimulated browning as assessed by histology, expression of uncoupling protein 1, and the induction of gene expression associated with browning. These effects were markedly attenuated when mice were treated with a β-blocker. Additionally, neither centrally nor peripherally administered FGF21 initiated browning in mice lacking β-adrenoceptors, demonstrating that an intact adrenergic system is necessary for FGF21 action. These data indicate that FGF21 can signal in the brain to activate the sympathetic nervous system and induce adipose tissue thermogenesis.

Sympathetic but not sensory denervation stimulates white adipocyte proliferation

2006 ◽  
Vol 291 (6) ◽  
pp. R1630-R1637 ◽  
Author(s):  
Michelle T. Foster ◽  
Timothy J. Bartness
Keyword(s):  
Sensory Nerve ◽  
Sympathetic Nerves ◽  
Cell Number ◽  
Sensory Nerves ◽  
Sensory Innervation ◽  
Fat Cell ◽  
Protein Marker ◽  
White Adipocyte ◽  
Sensory Denervation

White adipocyte proliferation is a hallmark of obesity, but it largely remains a mechanistic mystery. We and others previously demonstrated that surgical denervation of white adipose tissue (WAT) triggers increases in fat cell number, but it is unknown whether this was due to preadipocyte proliferation or maturation of existing preadipocytes that allowed them to be counted. In addition, surgical denervation severs not only sympathetic but also sensory innervation of WAT. Therefore, we tested whether sympathetic WAT denervation triggers adipocyte proliferation using 5-bromo-2′-deoxyuridine (BrdU) as a marker of proliferation and quantified BrdU-immunoreactive (ir) cells that were colabeled with AD-3-ir, an adipocyte-specific membrane protein marker. The unilateral denervation model was used for all experiments where Siberian hamster inguinal WAT (IWAT) was unilaterally denervated, the contralateral pad was sham denervated serving as a within-animal control, and then BrdU was injected systemically for 6 days. When IWAT was surgically denervated, severing both sympathetic and sensory nerves, tyrosine hydroxylase (TH)-ir, a sympathetic nerve marker, and calcitonin gene-related peptide (CGRP)-ir, a sensory nerve marker, were significantly decreased, and BrdU+AD-3-ir adipocytes were increased ∼300%. When IWAT was selectively sensory denervated via local microinjections of capsaicin, a sensory nerve-specific toxin, CGRP-ir, but not TH-ir, was decreased, and BrdU+AD-3-ir adipocytes were unchanged. When IWAT was selectively sympathetically denervated via local microinjections of 6-hydroxy-dopamine, a catecholaminergic-specific toxin, TH-ir, but not CGRP-ir, was significantly decreased, and BrdU+AD-3-ir adipocytes were increased ∼400%. Collectively, these data provide the first direct evidence that sympathetic nerves inhibit white adipocyte proliferation in vivo.

Effects of white adipose tissue grafts on total body fat and cellularity are dependent on graft type and location

2005 ◽  
Vol 289 (2) ◽  
pp. R380-R388 ◽  
Author(s):  
Eva L. Lacy ◽  
Timothy J. Bartness
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
White Adipose Tissue ◽  
Surgical Removal ◽  
Siberian Hamsters ◽  
Total Body Fat ◽  
Donor Graft ◽  
Total Body ◽  
Tissue Grafts ◽  
Autologous Grafts

Surgical removal of body fat (lipectomy) triggers compensatory increases in nonexcised white adipose tissue (WAT), thus restoring adiposity levels in many species, including Siberian hamsters. In Siberian hamsters, when their lipectomized WAT is transplanted to another site (autologous grafts, no net change in body fat), healthy grafts result, but the lipectomy-induced compensatory increases in nonexcised WAT masses are exaggerated, an effect that apparently occurs only when the grafts contact intact WAT. When WAT is added to nonlipectomized hamsters to increase body fat, native WAT pads do not decrease. Thus WAT addition or removal-replacement does not induce compensatory WAT responses consistent with total body fat regulation as does WAT subtraction. Therefore, we tested whether the exaggerated response to lipectomy occurring with autologous WAT transplantation is dependent on graft site placement and whether the donor graft source [inguinal or epididymal WAT (IWAT, EWAT), sibling vs. nonsibling] affected body fat responses to WAT additions in nonlipectomized hamsters. Lipectomized hamsters received subcutaneous autologous EWAT grafts placed remotely from other WAT (ventrum) or in contact with intact WAT (dorsum), whereas intact hamsters received EWAT or IWAT grafts from sibling or nonsibling donors. The exaggerated response to lipectomy only occurred when grafts were in contact with intact WAT. EWAT, but not IWAT, additions to nonlipectomized siblings or nonsiblings increased native IWAT and retroperitoneal WAT mass but not EWAT mass compared with controls. Collectively, WAT transplantation to either lipectomized or nonlipectomized hamsters increased body fat contingent on graft contact with intact or native WAT.

Sensory or sympathetic white adipose tissue denervation differentially affects depot growth and cellularity

2005 ◽  
Vol 288 (4) ◽  
pp. R1028-R1037 ◽  
Author(s):  
Haifei Shi ◽  
C. Kay Song ◽  
Antonio Giordano ◽  
Saverio Cinti ◽  
Timothy J. Bartness
Keyword(s):  
Adipose Tissue ◽  
Tyrosine Hydroxylase ◽  
Cell Size ◽  
White Adipose Tissue ◽  
Cell Number ◽  
Sensory Innervation ◽  
Fat Cell ◽  
Fat Cell Size ◽  
Total Fat ◽  
Differential Control

Functional and histological evidence for the sympathetic nervous system (SNS) innervation of white adipose tissue (WAT) exists for several species; however, its sensory innervation has only been shown in laboratory rats, and its function is unclear. We tested the effects of sensory and SNS innervation of Siberian hamster epididymal and inguinal WAT (EWAT and IWAT) by assessing calcitonin gene-related peptide (CGRP)- and tyrosine hydroxylase-immunoreactivity (ir), respectively. Next, we tested the role of the sensory innervation of WAT on growth and cellularity because WAT surgical denervation increases pad mass via selective increases in fat cell number, an effect ascribed to SNS denervation but that could be due to the accompanying surgical disruption of WAT sensory innervation. Sensory denervation was accomplished via multiple local microinjections of capsaicin into WAT, and its effects were compared with those of surgical denervation. Surgically denervated IWAT and EWAT showed significantly decreased tyrosine hydroxylase-ir and CGRP-ir, whereas capsaicin-treated WAT had only significantly decreased CGRP-ir. Surgically denervated pad masses were significantly increased; this was accompanied by increased total fat cell number in IWAT, with no change in fat cell size. EWAT only showed a significant increase in the number of small- to medium-sized adipocytes (75–125 μm diameter). By contrast, sensory-denervated pad masses were unchanged, but IWAT showed significantly increased average fat cell size. Collectively, these data provide immunohistochemical evidence for sensory and SNS innervation of WAT in Siberian hamsters and differential control of WAT cellularity by these innervations, as well as the ability of locally applied capsaicin to selectively reduce WAT sensory innervation.

Role of Development in Infant and Toddler Food Refusal

2010 ◽  
Vol 19 (3) ◽  
pp. 64-67
Author(s):  
Paul Hyman
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronically Ill ◽  
Oral Feeding ◽  
Sensory Innervation ◽  
Food Refusal ◽  
Behavioral Modification ◽  
Pain Stimuli ◽  
The Brain

The purpose of this manuscript is to inform clinicians working with infants who are tube fed about the brain-gut connections that may influence adaptation to oral feedings. Developmental changes in motility and sensory innervation are constant as brain and gut mature in the first several years. We hypothesized that chronically ill neonates are exposed to multiple pain stimuli during hospitalization, leaving them susceptible to hyperalgesia and chronic pain. Hyperalgesia in the abdomen, chest, pharynx, or face may be cause for food refusal. In patients who are tube fed who failed behavioral modification to teach eating, treatment of peripheral nerve and central nervous system hyperalgesia may be required before behavioral modification will work. We designed a 14 week outpatient protocol for moving infants and toddlers who are tube fed from tube to oral feeding using pain rehabilitation strategies. We used 8 weeks of post-pyloric feeding, eliminating stimuli to the oropharynx, esophagus, or stomach. We treated with amitriptyline and/or gabapentin to desensitize sensory receptors and central nervous system arousal. After 8 weeks, we gave the appetite stimulant megesterol for another 6 weeks. Five days after initiation of megesterol, we initiated a 1-hour/night schedule to withdraw tube feedings. In a small, uncontrolled study, all 9 children moved from tube to oral feedings.

Sign in / Sign up

Export Citation Format

Share Document