An important new study reveals that up to one in five people with prediabetes can return to normal blood sugar without losing weight, changing the way doctors are thinking of preventing type 2 diabetes.
Study: Prevention of type 2 diabetes through recession prediabetes with no weight loss. Credit Picture: Anna Rogalska/Shutterstock.com
In recent Natural medicine Article, the researchers investigated whether the protagonists can return to normal glucose regulation without losing weight, a finding that could be the key to preventing type 2 diabetes (T2D). They found that the recession prediabetes occurred despite weight loss (often with slight weight gain) and was associated with healthier fat distribution, improved β-cell function and enhanced insulin sensitivity.
Background
T2D affects over 460 million people worldwide and is the leading cause of death due to its complications, including neuropathy, cardiovascular disease and chronic kidney disease. The global weight of the T2D is expected to increase significantly by 2050. Poor nutrition quality is the main driver, with the greatest impact on low and medium -income countries with limited access to treatment. Prevention strategies are necessary to reduce the world weight of T2D.
Prediabetes is a metabolic condition in which blood sugar levels are higher than normal but not high enough to meet the diagnostic criteria for type 2 diabetes (T2D). It is usually defined by reduced glucose regulation, such as increased fasting glucose, weakened tolerance to glucose in an oral glucose tolerance test or increased glycozine glucovine (HBA1C), which falls below the threshold used to diagnose diabetes.
It is the most important risk factor for T2D. The annual development rate is 5-10%, with a risk of life up to ~ 74%. It also increases the risk of vascular, cancer and neurodegenerative diseases independently.
Previous research has shown that restoring normal glucose regulation, even temporarily, reduces the risk of developing T2D and related complications. The prediabetes lifestyle intervention study (PLIS) introduced the concept of prediabetes recession. The recession is achieved when normal glucose levels are restored, often through weight loss. This recession significantly reduces the risk of T2D and relative damage to the organ. This emphasizes the importance of regulating glucose in preventive strategies.
For the study
The researchers conducted a post -HOC analysis of PLI, a randomized, controlled, multicenter test conducted in Germany between 2012 and 2016. Participants were strained by the risk of diabetes based on insulin resistance, insulin secretion and liver
This analysis included only participants who did not lose weight for more than 12 months. If glucose regulation returned to normal, they were classified as correspondents and if they did not do so, they are classified as non -respondents.
Glucose metabolism was evaluated with oral glucose tolerance tests (OGTT) with repetitive blood sampling. Insulin, C-peptide, liver fat, visceral and subcutaneous fat and muscle fat were measured using standard tests, magnetic resonance imaging or spectroscopy. Additional analyzes included inflammatory markers, adipocins, indigenines and visceral ratings of polygonal risk of tissue (VAT), with no significant groups differences. Lifestyle attachment was followed through food calendars, gymnastics and physical activity evaluations.
The findings were validated in a second group from the US Diabetes Prevention Program, focusing on participants who also did not lose weight during the first 12 months. Statistical analyzes applied mixed results models and were corrected for multiple tests.
Basic findings
The study was followed by 1,105 people with PLIS prediabetes. Among the 234 participants who did not lose weight (or even won some) during the 12 -month program, 51 achieved recession while in 183 they did not. Specifically, the recession appeared regardless of changes in body weight, body composition, physical activity or aerobic ability.
Correspondents showed separate metabolic improvements. Their sensitivity to insulin has increased significantly, while non -respondents showed no change. In addition, respondents showed enhanced secretion of insulin and better beta-cell function, changes that were not typically observed in the recession with weight loss.
The distribution of body fat also differs: Correspondents store more fat in subcutaneous adipose tissue (SCAT), while avoiding VAT increases, leading to a higher Scat/Vat ratio. This healthier fat pattern was associated with higher levels of adiponectin, according to improved insulin sensitivity.
Other potential mechanisms, such as inflammation, liver accumulation or genetic predisposition, did not explain the recession. Specifically, correspondents had improved glycagon regulation and greater sensitivity of β-cells to glucogen-1 peptide-1, supporting better glucose control. In long -term monitoring, the recession without weight loss reduced the risk of T2D by ~ 71%, similar to the recession of weight loss. DPP confirmed these findings, enhancing their validity.
Conclusions
This study shows that up to 22% of participants can deliver prediabetes without weight loss and provides strong protection against T2D, comparable to the recession caused by weight. The main factor seems to be fat distribution: the correspondents accumulate more subcutaneously than visceral fat, which is associated with higher sensitivity to insulin, beta-cell function and improved GLP-1 sensitivity.
Exercise and nutritional composition may have contributed to these favorable results. The findings emphasize the need to extend the clinical guidelines beyond weight loss only, emphasizing the recession of normal glucose regulation as a primary prevention target.
The advantages include reproducing the results in the DPP group and detailed metabolic profile. The restrictions are post -hoc design, dependence on OGTT substitute measures and possible residual confusion.
Overall, the study emphasizes that metabolic health and glycemic downturn, not weight loss alone, should guide precision prevention strategies for T2D.
