ABSTRACT
Low levels of mitochondrial stress are beneficial for organismal health and survival through a process known as mitohormesis. Mitohormetic responses occur during or after exercise and may mediate some salutary effects of exercise on metabolism. Exercise-related mitohormesis involves reactive oxygen species production, mitochondrial unfolded protein response (UPRmt), and release of mitochondria-derived peptides (MDPs). MDPs are a group of small peptides encoded by mitochondrial DNA with beneficial metabolic effects. Among MDPs, mitochondrial ORF of the 12S rRNA type-c (MOTS-c) is the most associated with exercise. MOTS-c expression levels increase in skeletal muscles, systemic circulation, and the hypothalamus upon exercise. Systemic MOTS-c administration increases exercise performance by boosting skeletal muscle stress responses and by enhancing metabolic adaptation to exercise. Exogenous MOTS-c also stimulates thermogenesis in subcutaneous white adipose tissues, thereby enhancing energy expenditure and contributing to the anti-obesity effects of exercise training. This review briefly summarizes the mitohormetic mechanisms of exercise with an emphasis on MOTS-c.
ABSTRACT
Some patients with leprosy may present with atypical features, such as isolated peripheral neuropathy without skin lesions, or marked proprioceptive dysfunction. We report a 56-year-old female who presented with predominant proprioceptive loss without skin lesion, but was finally confirmed as leprous neuropathy by sural nerve biopsy. It is postulated that large myelinated fibers were affected by chronic immunological reactions triggered by inactive bacterial particles, producing a peripheral neuropathy presenting as predominant proprioceptive sensory loss without typical skin lesions.