Role of Prolactin in Brown Adipose Tissue Thermogenic Activity

Yahata, Takehiro; Kuroshima, Akihiro

doi:10.1007/978-3-0348-8491-4_53

Cited by 3 publications

(3 citation statements)

References 10 publications

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“…Yahata and Kuroshima [58] showed that in vitro glucagon-induced brown adipose tissue (BAT) thermogenesis in rats was suppressed by haloperidol and enhanced by bromocriptine; they suggested that PRL may inhibit nons hive ring thermogenesis. Chan and Swaminathan [67] showed that PRL is a possible mediator of BAT activity suppression during lactation.…”

Section: Prolactinmentioning

confidence: 99%

Endocrine Responses to Heat and Cold Stress

Matsumoto

Nishiyama

Nishimura

et al. 2001

Thermotherapy for Neoplasia, Inflammation, and Pain

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Summary. This review focuses on the endocrine responses to thermal stimuli during passive heat or cold exposure, with particular reference to the relation of these responses to the changes in the body core temperature (Teare). Mild to moderate hyperthermia (<1°C rise in Teare) induces the release of growth hormone and prolactin (PRL). Moderate hypothermia (la_2°C fall in Teore) suppresses PRL release. A positive correlation between plasma PRL and Teare suggests some role for PRL in thermoregulation. Hypothermia activates the hypothalamo-pituitary-thyroid (HPT) axis and releases thyrotropin-releasing hormone, thyroid-stimulating hormone (TSH), and thyroid hormones and increases the metabolic rate. Enhancement of extrathyroidal production of triiodothyronine (T3) from thyroxine (T4) may precede the TSH response to cold. Both severe hyperthermia and hypothermia (1°_3°C changes in Teare) activate the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system, resulting in release of corticotropin-releasing factor, adrenocorticotropic hormone, cortisol, and norepinephrine. The responses in the HPT axis and the HPA axis are not apparent in humans, as they are in rats, probably owing to the larger body mass of humans. Hyperthermia stimulates the renin-angiotensin-aldosterone system and the release of arginine vasopressin (AVP) and atrial natriuretic peptide, but this might be due to nonthermal factors. Diuresis due to suppression of AVP release is induced by cold. Gonadal response to thermal stimuli is possibly suppressive. The hormonal responses induced by thermal stress are mostly dependent on the change in Teare in humans; in small animals they are also dependent on the change in skin temperature. I ntrod uctionBody core temperature (Teare) may increase during physical exercise and passive heating (while sauna bathing, with head-out water immersion, and exposure to hot environments); it decreases during cold exposure. Changes in Teare induce various endocrine responses to maintain homeostasis of the body. Recently, local and whole-body hyperthermia therapy for cancer and some benign diseases and induced hypothermia treatment to protect the important organs from hypoxic damage have been developed and widely utilized. On these occasions, the endocrine responses induced by the changes in Teare should be considered. Hormonal responses and their relation to the immune system during exercise in the heat and passive hyperthermia have been reviewed [1][2][3], but little attention has been paid to the relation of endocrine responses to the change in Teare. Body heating and cooling paradigms may include concurrent psychological stress. This review focuses on the endocrine responses to thermal stimuli during passive heating and cooling, with particular reference to their relation to changes in Teare. The study was undertaken to elucidate the thermal influence alone, excluding the influence of non thermal stress. Growth HormoneThere have been many consistent findings that hyperthermia induces a rapid rise in ci...

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Section: Prolactinmentioning

confidence: 99%

Endocrine Responses to Heat and Cold Stress

Matsumoto

Nishiyama

Nishimura

et al. 2001

Thermotherapy for Neoplasia, Inflammation, and Pain

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“…The effect of glucagon on BAT may be suppressed by prolactin, probably through the inhibition of the intracellular signaling route via IP 3 ‐Ca 2+ , being important for NST stimulation by glucagon. It is assumed that glucagon plays a significant role when the responsiveness of BAT to NA is not fully established, such as the neonatal period and beginning stage of cold acclimation 5 …”

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confidence: 99%

“…It is assumed that glucagon plays a significant role when the responsiveness of BAT to NA is not fully established, such as the neonatal period and beginning stage of cold acclimation. 5 Aging attenuates cold-induced NST. It is probably caused by age-related reduction in BAT mass and the levels of mitochondrial GDP-binding (an index of active UCP) as well as UCP.…”

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confidence: 99%

Non‐shivering thermogenesis in brown adipose tissue and aging

Yahata

2004

Geriatrics Gerontology Int

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The aging-induced decrease in non-shivering thermogenic capacity was prevented in the genetically CCK-A receptor deficient, diabetic obese OLETF rats, provably by an increase in the responsiveness of BAT to glucagon. The potential metabolic capacities can be sustained until aged period. Body temperature is determined by the balance of heat dissipation from the body surface and respiration, and heat production. Under cold conditions, heat production is stimulated by shivering and non-shivering thermogenesis (thermogenesis without shivering: NST) in addition to the suppression of heat dissipation from the skin by cutaneous vasoconstriction, resulting in preventing hypothermia. During the process of cold acclimation, the heat production by NST substitutes for the one by shivering, and therefore a capacity for cold tolerance may mainly depend on the NST activity. The major factor stimulating NST is norepinephrine (NA) released from sympathetic nerves. 1 The major site of NST is brown adipose tissue (BAT). In contrast to usual adipose tissue (white adipose tissue), BAT is densely innervated with sympathetic nerves and is rich in vascular distribution. BAT is a unique tissue of which the sole task is thought to be heat production. 2 Norepinephrine acts on brown adipocytes via adrenergic b 3 receptor, causing the production of cAMP as an intracellular second messenger. cAMP activates protein kinase which is then followed by the activation of hormone-sensitive lipase, and finally hormonesensitive lipase resolves triglyceride. The free fatty acids (FFA) thus produced are transferred to the mitochondrion as a fuel, and the excess FFA as well as glycerol is released as a substrate for other tissues. Thermogenic activity of BAT is enhanced by cold exposure, overfeeding, adrenergic stimulation, and immobilization stress, and suppressed by heat exposure, obesity, and aging. 3 Brown adipocyte has numerous mitochondria, and the specific thermogenic activity of the cell is attributable to the restriction of oxidative phosphorylation by an uncoupling protein (UCP) on the inner membrane of the mitochondrion. In general, mitochondrial oxidation of fuels generates an electrochemical gradient via an outward pumping of protons by the electron transport chain. ATP production via ATP synthetase is then facilitated by the inward flux of protons down the gradient. However, in brown adipocyte mitochondrion the electrochemical gradient is counteracted by a proton influx via UCP, causing an uncoupling of oxidative phosphorylation, accompanied by the heat generation without ATP production. 4 Glucagon is a potent stimulator of BAT comparable with NA. The effect of glucagon on BAT may be suppressed by prolactin, probably through the inhibition of the intracellular signaling route via IP 3 -Ca 2+ , being important for NST stimulation by glucagon. It is assumed that glucagon plays a significant role when the responsiveness of BAT to NA is not fully established, such as the neonatal period and beginning stage of cold acclimation. 5 Aging attenuates...

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Polymorphism of winter phenotype in Siberian hamster: consecutive litters do not differ in photoresponsiveness but prolonged acclimation to long photoperiod inhibits winter molt

2021

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Background The theory of delayed life history effects assumes that phenotype of adult individual results from environmental conditions experienced at birth and as juvenile. In seasonal environments, being born late in the reproductive season affects timing of puberty, body condition, longevity, and fitness. We hypothesized that late-born individuals are more prone to respond to short photoperiod (SP) than early born ones. We used Siberian hamsters Phodopus sungorus, a model species characterized by high polymorphism of winter phenotype. We experimentally distinguished the effect of litter order (first or third) from the effect of exposure to long photoperiod (LP) before winter (3 months or 5 months) by manipulating the duration of LP acclimation in both litters. We predicted that, irrespective of the litter order, individuals exposed to long photoperiod for a short time have less time to gather energy resources and consequently are more prone to developing energy-conserving phenotypes. To assess effect of litter order, duration of acclimation to long days, and phenotype on basal cost of living we measured basal metabolic rate (BMR) of hamsters. Results Individuals born in third litters had faster growth rates and were bigger than individuals from first litters, but these differences vanished before transfer to SP. Litter order or duration of LP acclimation had no effects on torpor use or seasonal body mass changes, but prolonged acclimation to LP inhibited winter molting both in first and third litters. Moreover, individuals that did not molt had significantly higher BMR in SP than those which molted to white fur. Although one phenotype usually predominated within a litter, littermates were often heterogeneous. We also found that over 10% of individuals presented late response to short photoperiod. Conclusions Our data indicate that duration of postnatal exposure to LP may define propensity to photoresponsiveness, regardless of the litter in which animal was born. Existence of littermates presenting different phenotypes suggests a prudent reproductive strategy of investing into offspring of varied phenotypes, that might be favored depending on environmental conditions. This strategy could have evolved in response to living in stochastic environment.

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Role of Prolactin in Brown Adipose Tissue Thermogenic Activity

Cited by 3 publications

References 10 publications

Endocrine Responses to Heat and Cold Stress

Endocrine Responses to Heat and Cold Stress

Non‐shivering thermogenesis in brown adipose tissue and aging

Polymorphism of winter phenotype in Siberian hamster: consecutive litters do not differ in photoresponsiveness but prolonged acclimation to long photoperiod inhibits winter molt

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