Early Insulin Treatment Reduces Insulin Resistance
Sept 23, 2018 11:44:13 GMT -5
via mobile
goyocafe, thekindaguyiyam, and 8 more like this
Post by mnholdem on Sept 23, 2018 11:44:13 GMT -5
To Readers:
Several ProBoards members have asked where I discovered evidence that early insulin treatment restores beta cell output of insulin and reduces insulin resistance. This is one of many published articles on the subject.
INTRODUCTION OF INSULIN EARLIER IN THE TREATMENT PARADIGM
Typically, whereas introducing insulin therapy in a more timely fashion would significantly improve glycemic control among subjects with type 2 diabetes, the question of insulin initiation timing in relation to other antiglycemic therapies is the subject of considerable debate (10). While insulin administration has the potential of achieving the most effective reductions in glycemic control, the initiation of insulin therapy requires greater use of resources, time, and effort from provider and patient alike, compared with oral antidiabetic therapies (11). Patient resistance to the use of insulin therapy remains a challenge, especially in populations that may have misgivings and misconceptions regarding the role of insulin replacement in diabetes management.
Notwithstanding these issues, there are specific populations that would clearly benefit from early, aggressive, and targeted introduction of insulin therapy. For instance, patients presenting with significant hyperglycemia may benefit from timely initiation of insulin therapy that can effectively and rapidly correct their metabolic imbalance and reverse the deleterious effects of excessive glucose (glucotoxicity) and lipid (lipotoxicity) exposure on β-cell function and insulin action (12). In vitro studies have demonstrated that chronic hyperglycemia leads to increased production of reactive oxygen species, and subsequent oxidative stress, which appears to affect insulin promoter activity (PDX-1 and MafA binding) and results in diminished insulin gene expression in glucotoxic β-cells (13). Interestingly, in vitro experiments have shown that these glucotoxic effects occur in a continuum of glucose concentrations (no clear threshold effect), are reversible with reinstitution of euglycemic conditions, and result in the greatest recovery of β-cell function with shorter periods of exposure to hyperglycemia (14). Various studies have demonstrated improvement in insulin sensitivity and β-cell function after correction of hyperglycemia with intensive insulin therapy (15).
Source: www.ncbi.nlm.nih.gov/pmc/articles/PMC2811460/
Several ProBoards members have asked where I discovered evidence that early insulin treatment restores beta cell output of insulin and reduces insulin resistance. This is one of many published articles on the subject.
INTRODUCTION OF INSULIN EARLIER IN THE TREATMENT PARADIGM
Typically, whereas introducing insulin therapy in a more timely fashion would significantly improve glycemic control among subjects with type 2 diabetes, the question of insulin initiation timing in relation to other antiglycemic therapies is the subject of considerable debate (10). While insulin administration has the potential of achieving the most effective reductions in glycemic control, the initiation of insulin therapy requires greater use of resources, time, and effort from provider and patient alike, compared with oral antidiabetic therapies (11). Patient resistance to the use of insulin therapy remains a challenge, especially in populations that may have misgivings and misconceptions regarding the role of insulin replacement in diabetes management.
Notwithstanding these issues, there are specific populations that would clearly benefit from early, aggressive, and targeted introduction of insulin therapy. For instance, patients presenting with significant hyperglycemia may benefit from timely initiation of insulin therapy that can effectively and rapidly correct their metabolic imbalance and reverse the deleterious effects of excessive glucose (glucotoxicity) and lipid (lipotoxicity) exposure on β-cell function and insulin action (12). In vitro studies have demonstrated that chronic hyperglycemia leads to increased production of reactive oxygen species, and subsequent oxidative stress, which appears to affect insulin promoter activity (PDX-1 and MafA binding) and results in diminished insulin gene expression in glucotoxic β-cells (13). Interestingly, in vitro experiments have shown that these glucotoxic effects occur in a continuum of glucose concentrations (no clear threshold effect), are reversible with reinstitution of euglycemic conditions, and result in the greatest recovery of β-cell function with shorter periods of exposure to hyperglycemia (14). Various studies have demonstrated improvement in insulin sensitivity and β-cell function after correction of hyperglycemia with intensive insulin therapy (15).
Source: www.ncbi.nlm.nih.gov/pmc/articles/PMC2811460/