This research theme is aimed at sharing recent findings in the area of how type 1 and type 2 diabetes could precipitate non-alcoholic fatty liver disease (NAFLD) as well as other diabetes-driven liver pathologies. Of high interest and relevance is research that identifies how impaired glucose control and variability establishes a pathological liver homeostasis that may underlie the onset of NAFLD as well as other liver pathologies. For example, what are the potential mechanisms by which abnormal continuous excursions of glucose concentrations outside the normal ranges establish impaired hepatocyte function or the microvasculature of the liver together with hepatic tissue damage? What does such abnormal glycemic variability do to the formation of advanced glycation end products in hepatic tissues and how might this affect the progression towards NAFLD in an inflammation-dependent and independent manner?
Other topics of interest include how hepatic insulin resistance could on its own, or together with impaired glucose control and variability, precipitate liver pathology and how the onset of liver pathology could then directly or indirectly impair peripheral insensitivity. For example, how might abnormal glycemic variability precipitate systemic and/or hepatic inflammation and how might this influence peripheral and hepatic insulin sensitivity as well as possibly establishing hepatic pathology?
Of additional interest is research on methods that can co-regulate an improvement in *both* glucose control and variability and liver pathology *concomitantly* (i.e. is there a single pharmacologic agent that can concomitantly-improve insulin sensitivity and prevent hepatic pathology?).
For this special issue, primary research findings are highly encouraged, but insightful reviews on the themes indicated earlier will also be appropriate and highly-considered.
This research theme is aimed at sharing recent findings in the area of how type 1 and type 2 diabetes could precipitate non-alcoholic fatty liver disease (NAFLD) as well as other diabetes-driven liver pathologies. Of high interest and relevance is research that identifies how impaired glucose control and variability establishes a pathological liver homeostasis that may underlie the onset of NAFLD as well as other liver pathologies. For example, what are the potential mechanisms by which abnormal continuous excursions of glucose concentrations outside the normal ranges establish impaired hepatocyte function or the microvasculature of the liver together with hepatic tissue damage? What does such abnormal glycemic variability do to the formation of advanced glycation end products in hepatic tissues and how might this affect the progression towards NAFLD in an inflammation-dependent and independent manner?
Other topics of interest include how hepatic insulin resistance could on its own, or together with impaired glucose control and variability, precipitate liver pathology and how the onset of liver pathology could then directly or indirectly impair peripheral insensitivity. For example, how might abnormal glycemic variability precipitate systemic and/or hepatic inflammation and how might this influence peripheral and hepatic insulin sensitivity as well as possibly establishing hepatic pathology?
Of additional interest is research on methods that can co-regulate an improvement in *both* glucose control and variability and liver pathology *concomitantly* (i.e. is there a single pharmacologic agent that can concomitantly-improve insulin sensitivity and prevent hepatic pathology?).
For this special issue, primary research findings are highly encouraged, but insightful reviews on the themes indicated earlier will also be appropriate and highly-considered.
