Obesity is linked to numerous metabolic diseases, such as type 2 diabetes (T2D), non-alcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), some forms of cancer, infertility, Alzheimer's disease, frailty, and chronic kidney diseases. Insulin resistance (IR) is often considered a key underlying mechanism in these diseases.
IR can be understood as a physiological defense mechanism of the body that prevents the development of hypoglycemia to protect tissues from metabolic stress and nutrient-induced injury. However, increased IR is also one of the main pathogenic mechanisms for these metabolic diseases and conditions. Clinically, increased IR is defined as the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization in an individual as much as it does in a normal population.
It is established that increased IR is caused by a combination of genetic, epigenetic, and environmental factors (excess sugars or certain types of fatty acids, environmental pollutants, hormones released during psychological stress, obesity) and aging. Recent studies suggest that pharmacological interventions that decrease IR may reduce the risk of cancer and increase longevity. As the majority of societies are aging and the prevalence of obesity is increasing, there is an urgent need to identify mechanisms that slow down or decrease IR development during the lifespan in different health conditions, thus decreasing the progression of metabolic diseases and cancer, or ensuring more effective management of these conditions.
Furthermore, the prevalence of T2D is increasing worldwide, and the majority of patients with T2D have increased IR, which often continues to worsen after the diagnosis of T2D. Nevertheless, clear guidelines on how to manage decompensated T2D in patients treated with exogenous insulin who have severe IR are still lacking. Data from epidemiological studies suggesting that hyperinsulinemia itself is a risk factor for CVD and complications also prompt a re-evaluation of the approach to insulin therapy in patients showing signs of severe IR.
A better understanding of the molecular mechanisms related to IR will allow the selection of new treatment targets.
The topic aims to cover gaps or explore in more detail these fields but are not limited to:
• The causes of IR, including the role of various supplements, food additives, diets, medications, life events, gut microbiomes, physical inactivity, and aging.
• The relationship between IR and cognitive function, depression, heart failure, atherosclerosis, major CVD events, chronic kidney disease, obesity, NASH, and mortality.
• The measures that may decrease IR or delay IR progression (including metabolic diseases and aging) in persons with and without DM.
• The approach to dealing with severe IR in patients who are already treated with exogenous insulins.
• How to identify those T2D patients who should be reserved from exogenous insulin therapy when all oral and injectable antidiabetic medications are used but DM is uncontrolled.
• The T2DM treatment approach in cases of poor diabetes control in patients treated with insulin therapy plus oral/injectable antidiabetic medications due to advanced IR.
• The stratification of T2DM treatment approaches based on subgroups of adult-onset diabetes phenotypes.
• Investigating and understanding new molecular mechanisms related to IR.
• The association between food supplements, food additives, stress, new medications, aging, physical activity, microbiota, and IR.
• The relationship between IR and cognitive function, depression, heart failure, atherosclerosis, major CVD events, chronic kidney disease, obesity, NASH, and mortality.
• The T2DM treatment approach in cases of poor diabetes control in patients treated with insulin therapy plus oral/injectable antidiabetic medications due to advanced IR.
• The stratification of T2DM treatment approaches based on subgroups of adult-onset diabetes phenotypes.
Keywords:
Insulin resistance, aging, type 2 diabetes (T2D), Alzhaimer disease, cardiovascular disease, fatty liver, obesity, T2D management, T2D sub-types, exogenous insulin, food supplements, stress., Prediabetes, microRNA, epigenetic modifications, oxidative stress, sub-inflammation (low grade inflammation)
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Obesity is linked to numerous metabolic diseases, such as type 2 diabetes (T2D), non-alcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), some forms of cancer, infertility, Alzheimer's disease, frailty, and chronic kidney diseases. Insulin resistance (IR) is often considered a key underlying mechanism in these diseases.
IR can be understood as a physiological defense mechanism of the body that prevents the development of hypoglycemia to protect tissues from metabolic stress and nutrient-induced injury. However, increased IR is also one of the main pathogenic mechanisms for these metabolic diseases and conditions. Clinically, increased IR is defined as the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization in an individual as much as it does in a normal population.
It is established that increased IR is caused by a combination of genetic, epigenetic, and environmental factors (excess sugars or certain types of fatty acids, environmental pollutants, hormones released during psychological stress, obesity) and aging. Recent studies suggest that pharmacological interventions that decrease IR may reduce the risk of cancer and increase longevity. As the majority of societies are aging and the prevalence of obesity is increasing, there is an urgent need to identify mechanisms that slow down or decrease IR development during the lifespan in different health conditions, thus decreasing the progression of metabolic diseases and cancer, or ensuring more effective management of these conditions.
Furthermore, the prevalence of T2D is increasing worldwide, and the majority of patients with T2D have increased IR, which often continues to worsen after the diagnosis of T2D. Nevertheless, clear guidelines on how to manage decompensated T2D in patients treated with exogenous insulin who have severe IR are still lacking. Data from epidemiological studies suggesting that hyperinsulinemia itself is a risk factor for CVD and complications also prompt a re-evaluation of the approach to insulin therapy in patients showing signs of severe IR.
A better understanding of the molecular mechanisms related to IR will allow the selection of new treatment targets.
The topic aims to cover gaps or explore in more detail these fields but are not limited to:
• The causes of IR, including the role of various supplements, food additives, diets, medications, life events, gut microbiomes, physical inactivity, and aging.
• The relationship between IR and cognitive function, depression, heart failure, atherosclerosis, major CVD events, chronic kidney disease, obesity, NASH, and mortality.
• The measures that may decrease IR or delay IR progression (including metabolic diseases and aging) in persons with and without DM.
• The approach to dealing with severe IR in patients who are already treated with exogenous insulins.
• How to identify those T2D patients who should be reserved from exogenous insulin therapy when all oral and injectable antidiabetic medications are used but DM is uncontrolled.
• The T2DM treatment approach in cases of poor diabetes control in patients treated with insulin therapy plus oral/injectable antidiabetic medications due to advanced IR.
• The stratification of T2DM treatment approaches based on subgroups of adult-onset diabetes phenotypes.
• Investigating and understanding new molecular mechanisms related to IR.
• The association between food supplements, food additives, stress, new medications, aging, physical activity, microbiota, and IR.
• The relationship between IR and cognitive function, depression, heart failure, atherosclerosis, major CVD events, chronic kidney disease, obesity, NASH, and mortality.
• The T2DM treatment approach in cases of poor diabetes control in patients treated with insulin therapy plus oral/injectable antidiabetic medications due to advanced IR.
• The stratification of T2DM treatment approaches based on subgroups of adult-onset diabetes phenotypes.
Keywords:
Insulin resistance, aging, type 2 diabetes (T2D), Alzhaimer disease, cardiovascular disease, fatty liver, obesity, T2D management, T2D sub-types, exogenous insulin, food supplements, stress., Prediabetes, microRNA, epigenetic modifications, oxidative stress, sub-inflammation (low grade inflammation)
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.