Justin D. Crane

TL;DR: It is found that Tph1-deficient mice fed a high-fat diet (HFD) are protected from obesity, insulin resistance and nonalcoholic fatty liver disease (NAFLD) while exhibiting greater energy expenditure by BAT.

TL;DR: An obligatory role for skeletal muscle AMPK is demonstrated in maintaining mitochondrial capacity and contraction-stimulated glucose uptake, findings that were not apparent in mice with single mutations or deletions in muscle α, β, or γ subunits.

TL;DR: When administered to skeletal muscle that has been acutely damaged through exercise, massage therapy appears to be clinically beneficial by reducing inflammation and promoting mitochondrial biogenesis.

TL;DR: In response to a high-fat diet, iβ1β2AKO mice more rapidly developed liver steatosis as well as glucose and insulin intolerance, and AMPK in adipocytes is vital for maintaining mitochondrial integrity, responding to pharmacological agents and thermal stress, and protecting against nutrient-overload-induced NAFLD and insulin resistance.

TL;DR: Older adults have larger IMCL droplets, fewer mitochondria, and a lower proportion of IMCL in contact with mitochondria that likely contribute to age-related reductions in mitochondrial function and lipid metabolism.