Purpose of review
Cancer-related muscle loss, or cachexia, is the cause of death for approximately 2 million people worldwide and severely reduces quality of life. The degree of cachexia is inversely correlated with survival time; however, the exact mechanisms behind cancer-induced muscle wasting remain under investigation.
Recent findings
Cytokines such as TNF-α trigger degradatory pathways through NF-κB signaling that activate the ubiquitin-proteasome system and muscle proteolysis. Androgen treatment has been shown to reduce inflammatory cytokines and even stimulate anti-inflammatory cytokine production. Amino acid supplementation has been shown to induce muscle protein synthesis in ovarian cancer patients.
Summary
Targeted anabolic therapies aimed at preventing or reversing cancer cachexia might involve the combined use of androgens and amino acids working concurrently to enhance muscle protein synthesis and reduce muscle protein breakdown. Additional focused clinical studies are needed to identify muscle-specific targets or biomarkers for defined therapeutic approaches to slow or prevent cancer cachexia. In this paper we review the pathogenesis of cancer-related muscle wasting and discuss potential interventions at reversing or preventing cancer-related muscle loss.
Background: The real-world effect of intermittently scanned continuous glucose monitoring on glucose control in type 2 diabetes treated with basal insulin is uncertain. This retrospective real-world study aimed to evaluate change in glycated hemoglobin (HbA1c) amongst adults with type 2 diabetes managed with basal insulin starting flash glucose monitoring. Methods: Medical records were reviewed for adults with type 2 diabetes treated with basal insulin for ⩾1 year and using FreeStyle LibreTM Flash Glucose Monitoring for ⩾3 months. Prior to device use an HbA1c 8.0%–12.0% was recorded and a further HbA1c result was recorded 3–6 months (90–194 days) after starting device use. Results: Medical records ( n = 91) analyzed from six Canadian diabetes centers showed HbA1c significantly decreased by 0.8% ± 1.1 (mean ± SD, [ p < 0.0001]) from mean baseline HbA1c 8.9% ± 0.9 to 8.1% ± 1.0 at 3–6 months after initiating flash glucose monitoring. HbA1c improvement was not independently associated with age, BMI, insulin use duration, or sex. Conclusion: This Canadian real-world retrospective study showed significantly reduced HbA1c following initiation of flash glucose monitoring technology to further support management of type 2 diabetes treated with basal insulin.
There are scant prospective studies defining improvements in critical outcome measures with hormone replacement in hypopituitarism secondary to brain injury. We review the tests of cognition and physical function and summarize their use for subjects that are deficient in anterior hormone production during anterior pituitary hormone replacement in brain injury and propose these as the minimal tests that are feasible for a physician to perform in a clinical setting. We summarize the studies conducted to assess outcome measures after brain injury and also report preliminary findings for improvements in cognition and physical function in subjects with brain injury and GH deficiency.
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