Factors controlling brown adipose tissue development

Ricquier, Daniel; Mory, G.; Bouillaud, Frédéric; Combes-George, M.; Thibault, Jean; Blanchard, Christine

doi:10.1051/rnd:19850205

Cited by 10 publications

(5 citation statements)

References 3 publications

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“…The observation that BMR and total EE were increased to a similar extent in PTP-1B-deficient mice suggests an increase in adaptive thermogenesis, the process by which an organism dissipates excess energy as heat (41,50). Although there are many potential mechanisms for increased energy dissipation (see Discussion), in rodents, adaptive thermogenesis is often mediated by enhanced uncoupling of electron transport from oxidative phosphorylation (57,59,65). Uncoupling can be promoted by increased expression of UCPs in brown fat and/or skeletal muscle, the major thermogenic tissues in rodents (14,16,31,58).…”

Section: Resultsmentioning

confidence: 99%

“…Insulin may also influence metabolic rate by acting on the central nervous system. For example, insulin stimulation of hypothalamic neurons increases sympathetic stimulation of BAT, leading to an increase in energy expenditure (57,66). The major mechanism by which this occurs in rodents is by increasing brown fat mass and UCP expression (64).…”

Section: Discussionmentioning

confidence: 99%

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Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice

Klaman¹,

Boss²,

Peroni³

et al. 2000

Molecular and Cellular Biology

1,157

978

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Protein-tyrosine phosphatase 1B (PTP-1B) is a major protein-tyrosine phosphatase that has been implicated in the regulation of insulin action, as well as in other signal transduction pathways. To investigate the role of PTP-1B in vivo, we generated homozygotic PTP-1B-null mice by targeted gene disruption. PTP-1B-deficient mice have remarkably low adiposity and are protected from diet-induced obesity. Decreased adiposity is due to a marked reduction in fat cell mass without a decrease in adipocyte number. Leanness in PTP-1B-deficient mice is accompanied by increased basal metabolic rate and total energy expenditure, without marked alteration of uncoupling protein mRNA expression. In addition, insulin-stimulated whole-body glucose disposal is enhanced significantly in PTP-1B-deficient animals, as shown by hyperinsulinemic-euglycemic clamp studies. Remarkably, increased insulin sensitivity in PTP-1B-deficient mice is tissue specific, as insulin-stimulated glucose uptake is elevated in skeletal muscle, whereas adipose tissue is unaffected. Our results identify PTP-1B as a major regulator of energy balance, insulin sensitivity, and body fat stores in vivo.Obesity and diabetes mellitus represent major public health problems. Type 2 diabetes is a polygenic disease affecting over 100 million people worldwide. The risk of developing type 2 diabetes is increased in populations that lead a sedentary lifestyle and consume a typical western diet, in which more than 50% of the calories are derived from fat (34, 37). A high-fat diet and low energy expenditure predispose to obesity, a condition characterized by increased insulin resistance in insulinresponsive tissues, such as skeletal muscle, liver, and white adipose tissue (9, 42). Body weight also is subject to polygenic regulation (18). Many of the key genes that regulate body mass and glucose homeostasis remain to be identified (27).Insulin plays a critical role in regulating glucose homeostasis, lipid metabolism, and energy balance. Insulin signaling is initiated by binding of insulin to the insulin receptor (IR), a receptor tyrosine kinase. Insulin binding evokes a cascade of phosphorylation events, beginning with the autophosphorylation of the IR on multiple tyrosyl residues. Autophosphorylation enhances IR kinase activity and triggers downstream signaling events. These include tyrosyl phosphorylation of IR substrate (IRS) proteins (IRS-1 to -4) and other adapter molecules (e.g., Grb2 and Shc), whose combined actions mediate the biological effects of insulin (reviewed in references 24, 43, 54, and 69).

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice

Klaman¹,

Boss²,

Peroni³

et al. 2000

Molecular and Cellular Biology

1,157

978

View full text Add to dashboard Cite

show abstract

“…Thus, the effect of leptin following maternal PRL infusion may be mediated indirectly via stimulation of the sympathetic nervous system (Commins et al 1999b). A stimulatory effect of leptin on brown adipose tissue function acting via increased norepinephrine secretion would act to increase UCP1 abundance (Ricquier & Mory 1984) at the same time as lipid content declines as a consequence of enhanced lipolysis.…”

Section: Discussionmentioning

confidence: 99%

The effect of maternal prolactin infusion during pregnancy on fetal adipose tissue development

Budge¹,

Mostyn²,

Wilson³

et al. 2002

Journal of Endocrinology

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The present study determines whether maternal administration of prolactin (PRL) to dams promotes the abundance of the brown adipose tissue-specific uncoupling protein-1 (UCP1) in fetal and neonatal rat pups. Recombinant PRL (24 µg/kg per day), or an equivalent volume of saline, were infused into dams (n=19 per group) throughout pregnancy from 12 h after mating. Interscapular brown adipose tissue was sampled either from fetuses at 19·5 days of gestation (term=21·5 days) or from neonatal rat pups at approximately 18 h after birth. The abundance of UCP1 was determined by immunoblotting on adipose tissue samples from individual pups and pooled from groups of pups. This analysis was complemented by immunocytochemistry on representative adipose tissue samples. Maternal PRL infusion resulted in a greater abundance of UCP1 in fetal rats at 19·5 days of gestation (control: 97·2 8·4% reference; PRL: 525·6 74·4% reference; P<0·001) and in neonates 18 h after birth. In contrast, the abundance of the outer mitochondrial membrane protein voltage-dependent anion channel was unaffected by PRL. Neonatal adipose tissue sampled from pups born to PRL-infused dams possessed fewer lipid droplets, but more UCP1, as determined by immunocytochemistry. Fetal, but not maternal, plasma leptin concentrations were also increased by maternal PRL administration. In conclusion, as rats are altricial, and the potential thermogenic activity of brown adipose tissue develops over the first few days of postnatal life, these changes prior to, and at the time of, birth implicate PRL in fetal and neonatal adipose tissue maturation.

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“…The sympathetic nervous system is thought to mediate the chronic adaptative changes in brown adipose tissue during cold-acclimation (for review see Ricquier et al, 1985). However, early attempts to mimic chronic sympathetic stimulus by repetitive noradrenaline injection were largely unsuccessful (LeBlanc & Villemaire, 1970;Desautels & Himms-Hagen, 1979;Mory et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Induction of functional uncoupling protein in guinea pigs infused with noradrenaline. Studies with isolated brown adipocytes

Cunningham

Nicholls

1987

Biochemical Journal

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Continuous infusion of noradrenaline over the interscapular brown fat of guinea pigs maintained at thermoneutrality (28-32 degrees C) induces changes similar to those after cold-adaptation. (1) Multilocular fat droplets appear within the brown adipocytes. (2) The number of mitochondria per adipocyte and the total number of adipocytes both increase. (3) Noradrenaline addition to isolated adipocytes causes near maximal uncontrolled respiration. (4) The cells become more sensitive to fatty acid-induced uncoupling. (5) The tissue-specific uncoupling protein per mg of mitochondrial protein is increased 5-fold. Specific alpha- and beta-agonists were also chronically infused. (6) Separate infusion of phenylephrine or isoprenaline was not able to stimulate mitochondriogenesis or hyperplasia. (7) Adipocytes from these animals could not be uncoupled by acute noradrenaline. (8) Simultaneous chronic infusion of phenylephrine and isoprenaline reproduced the effects of chronic noradrenaline infusion.

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Factors controlling brown adipose tissue development

Cited by 10 publications

References 3 publications

Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice

Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice

The effect of maternal prolactin infusion during pregnancy on fetal adipose tissue development

Induction of functional uncoupling protein in guinea pigs infused with noradrenaline. Studies with isolated brown adipocytes

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