Neuropeptide and noradrenaline distributions in rat interscapular brown fat and in its intact and obstructed nerves of supply

Lever, J. D.; Mukherjee, Sagarika; Norman, David; Symons, Debbie; Jung, R. T.

doi:10.1016/0165-1838(88)90003-3

Cited by 30 publications

(12 citation statements)

References 16 publications

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“…The sympathetic nervous system is the major effector of thermogenesis through the release of noradrenaline from nerve endings present in both vessels and adipocytes [28,29]. In brown adipose tissue, noradrenaline, mainly through β-receptors, activates proliferation [30,31] and induces the uncoupling protein-1 (UCP-1) expression [32].…”

Section: Discussionmentioning

confidence: 99%

Resistance to obesity in Lou/C rats prevents ageing-associated metabolic alterations

et al. 2003

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Aims/Hypothesis. Ageing is associated with metabolic alterations characterised by changes in energy expenditure, obesity, leptin and insulin resistance. The Lou/C rat, an inbred strain of Wistar origin, is presented as both an obesity-resistant rat and a model of healthy ageing. Methods. To characterise the mechanisms underlying obesity resistance in Lou/C rat, we measured food intake and energy expenditure by indirect calorimetry at 1, 6, 12, 18, and 24 months of age. Moreover, plasma insulin and leptin concentrations were assessed by radioimmunoassay in Lou/C and Wistar rats throughout their life span. Results. Compared to Wistar rats, Lou/C rats presented a higher food intake only at 24 months of age and they had a higher energy expenditure at 6 and 12 months of age (+21% and +14%, respectively). Plasma insulin concentration increased markedly in 18-and 24-month-old Wistar rats, but remained stable during ageing in Lou/C rats. From the age of 6 months, the plasma leptin concentrations in Wistar rats were higher than in Lou/C rats of the same age (four-, seven-, five-and threefold higher at 6, 12, 18, 24 months of age, respectively). Conclusion/interpretation. Compared to Wistar rats, Lou/C rats did not develop insulin resistance as confirmed by a higher glucose infusion rate during the hyperinsulinaemic-euglycaemic clamp. These data provide evidence that insulin resistance is associated with the excess of adipose tissue in Wistar rats. Not only Lou/C rats present a higher median life span than Wistar rats (+20%), but they also show a healthy ageing process considering fat accretion and insulin resistance. [Diabetologia (2003[Diabetologia ( ) 46:1489[Diabetologia ( -1496 Keywords Insulin resistance, energy expenditure, leptin, ageing, Lou/C rat, food intake. lin. Insulin is considered as an adiposity signal. Its plasma concentration is associated with the amount of fat stores [1,2] and insulin receptors are expressed in the brain, especially in the paraventricular nuclei involved in the control of energy intake [3,4]. Insulin resistance is associated with fat accretion [5] and/or with the effect of ageing on the insulin receptor [6]. Leptin, which is secreted by adipocytes, provides feedback information on the lipid stores towards the hypothalamus. Leptin contributes to the regulation of both food intake and energy expenditure [7,8]. The plasma leptin concentration is directly related to body fat mass [9,10] but during ageing, increased concentrations of plasma leptin appears dissociated from fat stores [11]. However, it is extremely difficult to differAgeing is associated with metabolic disorder characterised notably by changes in energy expenditure, fat distribution leading to increased adiposity and insulin resistance.Several hormones can affect both energy expenditure and fat mass, amongst which are leptin and insu-

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Section: Discussionmentioning

confidence: 99%

Resistance to obesity in Lou/C rats prevents ageing-associated metabolic alterations

et al. 2003

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“…Furthermore, several studies (Cannon et al, 1986;Lever et al, 1988Lever et al, , 1989Norman et al, 1988) have suggested that some neuropeptides occur in nerves supplying IBAT and PBAT. Thus, the neural control of BAT is more complex than previously thought and includes both sympathetic and sensory nerves (reviewed in HimmsHagen, 1991).…”

Section: Introductionmentioning

confidence: 99%

Tyrosine hydroxylase, neuropeptide Y, substance P, calcitonin gene-related peptide and vasoactive intestinal peptide in nerves of rat periovarian adipose tissue: an immunohistochemical and ultrastructural investigation

et al. 1996

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Rat periovarian adipose tissue contains unilocular adipocytes and some multilocular adipocytes that, following acclimation to cold, become more numerous and give rise to periovarian brown fat areas. We studied the occurrence and distribution of tyrosine hydroxylase, neuropeptide Y, substance P, calcitonin gene-related peptide, vasoactive intestinal peptide, methionine enkephalin, neurotensin, galanin, and cholecystokinin 9-20 in the nerves of rat periovarian tissue maintained at 20 degrees C (control rats), acclimated at 4 degrees C (cold acclimated rats) and at 28 degrees C (warm-acclimated rats). In the periovarian tissue of control and warm-acclimated rats, tyrosine hydroxylase-like, neuropeptide Y-like, substance P-like and calcitonin gene-related peptide-like immunoreactive elements (putative nerves) were present in the blood vessels. In the periovarian tissue of cold-acclimated rats, we found: (1) a more widespread vascular distribution of these neuropeptides; (2) tyrosine hydroxylase-like and calcitonin gene-related peptide-like immunoreactive elements among paucilocular and multilocular adipocytes (parenchymal-like nerves); (3) vasoactive intestinal peptide-like immunoreactive elements in some arteries. Investigation by EM showed the presence of heterogeneous non-myelinated axons both associated with capillaries and among paucilocular and multilocular adipocytes (parenchymal fibres) in periovarian brown fat areas. In conclusion, periovarian brown fat contains the same neuropeptides, with the same vascular and parenchymal distribution, already seen in typical depots of brown fat.

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“…However, the failure of NPY to modulate the cAMP production, oxygen consumption and also ERK activation suggests that functional NPY receptors are lacking in brown adipocytes. Therefore, it is unlikely that NPY directly controls basal and NE-regulated thermogenesis in a short period of time, even if some sympathetic nerves carrying both NE and NPY innervate brown adipocytes [23,28,38].…”

Section: Discussionmentioning

confidence: 99%

“…The co-existence of sympathetic and peptidergic innervation has been demonstrated in BAT [5,11,23,28,38]. Among peptidergic neurotransmitters, neuropeptide Y (NPY) levels in the BAT are significantly decreased and increased by surgical excision of the sympathetic nerves to the BAT and putting an animal into a cold environment, respectively [30].…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, it is suggested that NPY co-localizes with tyrosine hydroxylase in noradrenergic neurons, but only in the perivascular nerve fiber network [11]. However, other studies showed that NE-and NPY-positive fibers were also found around parenchymal brown adipocytes in mice [38] and rats [23,28]. 4 NPY exhibits its physiological effects through at least four receptors known as Y1, Y2, Y4, and Y5.…”

Section: Introductionmentioning

confidence: 99%

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Neuropeptide Y activates phosphorylation of ERK and STAT3 in stromal vascular cells from brown adipose tissue, but fails to affect thermogenic function of brown adipocytes

et al. 2012

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Neuropeptide and noradrenaline distributions in rat interscapular brown fat and in its intact and obstructed nerves of supply

Cited by 30 publications

References 16 publications

Resistance to obesity in Lou/C rats prevents ageing-associated metabolic alterations

Resistance to obesity in Lou/C rats prevents ageing-associated metabolic alterations

Tyrosine hydroxylase, neuropeptide Y, substance P, calcitonin gene-related peptide and vasoactive intestinal peptide in nerves of rat periovarian adipose tissue: an immunohistochemical and ultrastructural investigation

Neuropeptide Y activates phosphorylation of ERK and STAT3 in stromal vascular cells from brown adipose tissue, but fails to affect thermogenic function of brown adipocytes

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