Mild Physiologic Hyperglycemia Induces Hepatic Insulin Resistance in Healthy Normal Glucose Tolerant Subjects–Role of Glucagon and Gluconeogenic Substrates

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 41-OR
Author(s):  
DEVJIT TRIPATHY ◽  
AURORA MEROVCI ◽  
ENRIQUE R. MALDONADO CORCHADO ◽  
BASU RITA ◽  
RALPH A. DEFRONZO
Keyword(s):  
Insulin Resistance ◽  
Hepatic Insulin Resistance ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Gluconeogenic Substrates

scholarly journals Mild Physiologic Hyperglycemia Induces Hepatic Insulin Resistance in Healthy Normal Glucose-Tolerant Participants

2019 ◽  
Vol 104 (7) ◽  
pp. 2842-2850 ◽  
Author(s):  
Devjit Tripathy ◽  
Aurora Merovci ◽  
Rita Basu ◽  
Muhammad Abdul-Ghani ◽  
Ralph A DeFronzo
Keyword(s):  
Insulin Resistance ◽  
Hepatic Insulin Resistance ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant

scholarly journals The Relationship between Serum Ferritin and Insulin Resistance in Different Glucose Metabolism in Nonobese Han Adults

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Bo-wei Liu ◽  
Xu-min Xuan ◽  
Jun-ru Liu ◽  
Fang-ning Li ◽  
Fu-Zai Yin
Keyword(s):  
Insulin Resistance ◽  
Serum Ferritin ◽  
Elevated Serum ◽  
Ferritin Concentration ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Han Adults ◽  
Diagnosed Diabetes ◽  
Newly Diagnosed Diabetes

The exact mechanism through which elevated serum ferritin promotes the development of type 2 diabetes is unknown. This study showed that ferritin concentration in impaired glucose regulation and newly diagnosed diabetes mellitus subjects of nonobesity already significantly increased when compared with normal glucose tolerant subjects of nonobesity. Elevated serum ferritin levels are associated with insulin resistance and may be not associated with the decline of insulin beta cells in different status of glucose tolerance in nonobese Han adults.

Mild Physiologic Hyperglycemia Impairs Beta-Cell Function and Induces Insulin Resistance in Healthy Normal Glucose Tolerant Subjects

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1827-P
Author(s):  
AURORA MEROVCI ◽  
ENRIQUE R. MALDONADO CORCHADO ◽  
DEVJIT TRIPATHY ◽  
RALPH A. DEFRONZO
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant

scholarly journals Risk of Insulin Resistance in Normal Glucose Tolerant Subjects

2019 ◽  
Vol 02 (01) ◽  
pp. 12-14
Author(s):  
Dr.Shiva kumar ◽  
Dr Bhargavi SK ◽  
Dr Lakshmi D ◽  
Dr Sathisha TG ◽  
Dr Hamsaveena
Keyword(s):  
Insulin Resistance ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant

scholarly journals Role of Insulin Resistance in MAFLD

2021 ◽  
Vol 22 (8) ◽  
pp. 4156
Author(s):  
Yoshitaka Sakurai ◽  
Naoto Kubota ◽  
Toshimasa Yamauchi ◽  
Takashi Kadowaki
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
De Novo Lipogenesis ◽  
Hepatic Insulin Resistance ◽  
Metabolic Dysfunction ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation

Many studies have reported that metabolic dysfunction is closely involved in the complex mechanism underlying the development of non-alcoholic fatty liver disease (NAFLD), which has prompted a movement to consider renaming NAFLD as metabolic dysfunction-associated fatty liver disease (MAFLD). Metabolic dysfunction in this context encompasses obesity, type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome, with insulin resistance as the common underlying pathophysiology. Imbalance between energy intake and expenditure results in insulin resistance in various tissues and alteration of the gut microbiota, resulting in fat accumulation in the liver. The role of genetics has also been revealed in hepatic fat accumulation and fibrosis. In the process of fat accumulation in the liver, intracellular damage as well as hepatic insulin resistance further potentiates inflammation, fibrosis, and carcinogenesis. Increased lipogenic substrate supply from other tissues, hepatic zonation of Irs1, and other factors, including ER stress, play crucial roles in increased hepatic de novo lipogenesis in MAFLD with hepatic insulin resistance. Herein, we provide an overview of the factors contributing to and the role of systemic and local insulin resistance in the development and progression of MAFLD.

scholarly journals Caloric Restriction Reverses Hepatic Insulin Resistance and Steatosis in Rats with Low Aerobic Capacity

Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5157-5164 ◽  
Author(s):  
Thomas A. Bowman ◽  
Sadeesh K. Ramakrishnan ◽  
Meenakshi Kaw ◽  
Sang Jun Lee ◽  
Payal R. Patel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Caloric Restriction ◽  
Visceral Obesity ◽  
Insulin Clearance ◽  
Hepatic Insulin Resistance ◽  
The Metabolic Syndrome ◽  
Cell Adhesion Molecule 1 ◽  
Muscle Triglyceride

Rats selectively bred for low aerobic running capacity exhibit the metabolic syndrome, including hyperinsulinemia, insulin resistance, visceral obesity, and dyslipidemia. They also exhibit features of nonalcoholic steatohepatitis, including chicken-wire fibrosis, inflammation, and oxidative stress. Hyperinsulinemia in these rats is associated with impaired hepatic insulin clearance. The current studies aimed to determine whether these metabolic abnormalities could be reversed by caloric restriction (CR). CR by 30% over a period of 2–3 months improved insulin clearance in parallel to inducing the protein content and activation of the carcinoembryonic antigen-related cell adhesion molecule 1, a main player in hepatic insulin extraction. It also reduced glucose and insulin intolerance and serum and tissue (liver and muscle) triglyceride levels. Additionally, CR reversed inflammation, oxidative stress, and fibrosis in liver. The data support a significant role of CR in the normalization of insulin and lipid metabolism in liver.

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