Reviews
| Rev Diabet Stud,
2011,
8(4):446-453 |
DOI 10.1900/RDS.2011.8.446 |
Beta-Cell Preservation…Is Weight Loss the Answer?
Angela D. Mazza1, Richard E. Pratley1,2, Steven R. Smith1,2
1Florida Hospital Diabetes Institute, Translational Research Institute for Metabolism and Diabetes, 2566 Lee Road, Winter Park, Orlando, Florida 32789, USA
2Sanford-Burnham Medical Research Institute, Orlando, Florida, USA
Address correspondence to: Angela D. Mazza, e-mail: angela.mazza.do@flhosp.org
Abstract
Obesity is associated with an increased risk of type 2 diabetes (T2D). Pancreatic beta-cell failure is an early event in the development of glucose dysregulation and diabetes. Interventions to halt beta-cell failure in T2D include diet modification, exercise, and use of pharmacologic agents. There is evidence that abdominal obesity may contribute to diabetes through insulin resistance and beta-cell impairment. Pivotal long-term studies into the prevention of T2D have shown the importance of weight loss beside diet, lifestyle, and medication. The Finnish Diabetes Prevention Program (DPP) showed that weight loss gradually reduces the risk of diabetes, and that even modest weight loss can significantly reduce the incidence of T2D. Similarly, in the US DPP, weight loss as part of intensive lifestyle modification was the major factor in reducing the incidence of T2D in high-risk subjects, being more effective than drug intervention. While understanding the relationship between obesity and diabetes is complex, we know that weight loss has positive effects on adipose tissue. It causes an increase in the beneficial fat cell hormone adiponectin, and a decrease in adipose tissue inflammation. Also, it is associated with reduced insulin resistance and a consequential reduction in glucolipotoxicity, which can improve beta-cell function. In summary, weight loss improves glycemic control and thereby mitigates diabetes symptoms and complications, possibly through the preservation of beta-cell function. Therefore, efforts to prevent diabetes and preserve beta-cell function in patients with T2D should more rigorously emphasize and target weight loss.
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| Rev Diabet Stud,
2011,
8(4):454-467 |
DOI 10.1900/RDS.2011.8.454 |
Hepatic Steatosis in Type 1 Diabetes
Simon E. Regnell, Ake Lernmark
Lund University, CRC, Department of Clinical Sciences, Diabetes and Celiac Disease Unit, Skane University Hospital, SUS SE-20502, Malmö, Sweden
Address correspondence to: Simon E. Regnell, e-mail: fek09sre@student.lu.se
Abstract
Islet autoimmunity in type 1 diabetes results in the loss of the pancreatic β-cells. The consequences of insulin deficiency in the portal vein for liver fat are poorly understood. Under normal conditions, the portal vein provides 75% of the liver blood supply. Recent studies suggest that non-alcoholic fatty liver disease (NAFLD) may be more common in type 1 diabetes than previously thought, and may serve as an independent risk marker for some chronic diabetic complications. The pathogenesis of NAFLD remains obscure, but it has been hypothesized that hepatic fat accumulation in type 1 diabetes may be due to lipoprotein abnormalities, hyperglycemia-induced activation of the transcription factors carbohydrate response element-binding protein (ChREBP) and sterol regulatory element-binding protein 1c (SREBP-1c), upregulation of glucose transporter 2 (GLUT2) with subsequent intrahepatic fat synthesis, or a combination of these mechanisms. Novel approaches to non-invasive determinations of liver fat may clarify the consequences for liver metabolism when the pancreas has ceased producing insulin. This article aims to review the factors potentially contributing to hepatic steatosis in type 1 diabetes, and to assess the feasibility of using liver fat as a prognostic and/or diagnostic marker for the disease. It provides a background and a case for possible future studies in the field.
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