Refeeding and insulin increase lipoprotein lipase activity in rat brown adipose tissue

Induction of lipoprotein lipase activity in brown adipose tissue (BAT) in response to cold stress has earlier been shown to be regulated by a beta-adrenergic mechanism and to be dependent on mRNA synthesis. In the present study, we have investigated the acute effects of refeeding after a short starvation period and the hormonal mechanism underlying the observed effects. Refeeding was found to rapidly increase tissue wet weight and lipoprotein lipase activity. The increase in enzyme activity could be blocked by the RNA synthesis inhibitor actinomycin D, indicating a gene activation. beta-Adrenergic blockade had no effect on this elevation of enzyme activity, but the increase could be mimicked by insulin injection. The results suggest that BAT contains two different pathways for regulation of lipoprotein lipase activity, both involving mRNA synthesis.

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Beta-adrenergic stimulation of lipoprotein lipase in rat brown adipose tissue during acclimation to cold

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1984.246.4.e327 ◽

1984 ◽

Vol 246 (4) ◽

pp. E327-E333 ◽

Cited By ~ 7

Author(s):

C. Carneheim ◽

J. Nedergaard ◽

B. Cannon

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Protein Content ◽

Lipoprotein Lipase ◽

Lipase Activity ◽

Lipoprotein Lipase Activity ◽

Beta Adrenergic ◽

Brown Adipose ◽

Adrenergic Mechanism ◽

Wet Weight

Lipoprotein lipase activity in adult rats was investigated in animals subjected to cold and to different hormonal treatments. In contrast to changes in tissue wet weight and total protein content, which showed a lag time of about 1 day, lipoprotein lipase activity was markedly (fourfold) increased after only 4 h in the cold. Total lipoprotein lipase activity reached a plateau already after 1-3 days, whereas wet weight and protein content did not plateau until 3 wk. Neither insulin nor glucose injections could mimic the cold-induced increase in lipoprotein lipase activity seen after 4 h. However, the effect of norepinephrine injections was identical to the effect of cold. The beta-agonist isoprenaline was as effective as norepinephrine, whereas the alpha-agonist phenylephrine had no effect. The beta-antagonist propranolol inhibited the cold-induced increase in lipoprotein lipase activity. It is concluded that, in contrast to white adipose tissue, brown adipose tissue lipoprotein lipase is stimulated in vivo by a beta-adrenergic mechanism and that it is this beta-adrenergic mechanism that is responsible for the rapid recruitment of lipoprotein lipase during cold exposure.

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Cold-induced beta-adrenergic recruitment of lipoprotein lipase in brown fat is due to increased transcription

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.254.2.e155 ◽

1988 ◽

Vol 254 (2) ◽

pp. E155-E161 ◽

Cited By ~ 4

Author(s):

C. Carneheim ◽

J. Nedergaard ◽

B. Cannon

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cholera Toxin ◽

Lipoprotein Lipase ◽

Lipase Activity ◽

Half Life ◽

Lipoprotein Lipase Activity ◽

Synthesis Inhibitor ◽

Beta Adrenergic ◽

Brown Adipose

The cellular basis for the cold-induced increase in lipoprotein lipase activity in rat brown adipose tissue was investigated. Rats were treated with inhibitory agents and either exposed to cold for 4 h or injected with isoprenaline. Lipoprotein lipase activity was followed in acetone-ether extracts of the tissue. Besides cold, both the beta-adrenergic agonist isoprenaline and the adenylate cyclase activator cholera toxin were able to increase lipoprotein lipase activity in the tissue. The protein synthesis inhibitor cycloheximide fully abolished this response; the half-life of lipoprotein lipase activity was both in control and in the cold-exposed state approximately 2 h. Also the mRNA synthesis inhibitor actinomycin D fully abolished the cold-, the isoprenaline-, and the cholera toxin-induced increases in lipoprotein lipase activity; the half-life of lipoprotein lipase mRNA was estimated to be 20-30 h. However, in animals returned to control conditions after a 4-h cold stress, the decline in activity corresponded to a half-life of only 4 h. It was concluded that the increase in lipoprotein lipase activity in the brown adipose tissue of cold-exposed rats is not due to an activation of preexisting enzyme nor due to an increased half-life of functional enzyme. Rather it is suggested that in brown adipose tissue the rate of lipoprotein lipase gene transcription is positively regulated by the cellular level of cAMP and that this increase in lipoprotein lipase mRNA leads directly to an increased rate of enzyme synthesis and hence to the increase in activity.

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