{'fraction_non_alphanumeric': 0.012048192771084338, 'fraction_numerical': 0.007228915662650603, 'mean_word_length': 5.811475409836065, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Physiological Significance of Mitochondrial Uncoupling Protein 1 in the Prevention of Reactive Oxygen Species and Control of Substrate Oxidation

The established function of mitochondrial uncoupling protein 1 in mammalian brown adipose tissue is the dissipation of proton motive force as heat. Uncoupling of respiration may also prevent mitochondrial superoxide production and ROS formation, but the involvement of UCP1 in this process is highly disputed. We here studied in isolated mitochondria a) whether the presence of endogenous uncoupling protein 1 in brown adipose tissue affects superoxide production, in particular during cold acclimation and beta oxidation, b) whether ectopically expressed UCP1 in skeletal muscle is functional and manipulates superoxide, and c) how substrate oxidation adapts to the presence of UCP1.