Fasting’s Effectiveness in Combating Insulin Resistance in Type 2 Diabetes
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中文書、漫畫輕小說5折起、電子書35元起，全館滿$1,000送100點金幣
內容簡介
More than 34 million Americans suffer from diabetes, and 88 million adults are considered prediabetic. The majority of these cases, around 90-95%, are diagnosed as Type 2 Diabetes Mellitus (T2DM) (Center for Disease Control and Prevention [CDC], 2019). In the United States alone, the prevalence of obesity has risen from 30.5% in 1999-2000 to 42.4% in 2017-2018 (CDC, 2021). This increase in obesity, along with T2DM, has also led to a rise in related conditions such as cardiovascular disease, stroke, and fatalities associated with these diseases. The roots of the obesity epidemic can be traced back to an event over 50 years ago when the sugar industry allegedly influenced scientists and researchers to shift the blame for poor health onto dietary fat (National Public Radio, 2016). This belief resulted in the proliferation of "fat-free" food products in grocery stores, shaping the development of the Western Diet characterized by excessive consumption of sugar and processed food (Kopp, 2019).
Foods that are high in carbohydrates but low in dietary fat and protein offer limited satiety, making it easier to overconsume them (Tremblay & Bellisle, 2015). Chronic consumption of both high-carbohydrate and high-fat foods eventually leads to the development of insulin resistance (IR) and T2DM (Khathi et al., 2018). IR is characterized by the body's inability to effectively utilize insulin, whether endogenous or exogenous, to facilitate glucose uptake (Lebovitz, 2001). T2DM is closely associated with IR and can be defined as the dysfunction of beta cells, resulting in elevated blood sugar levels (hyperglycemia).
The Diverse Effects of Insulin Resistance (IR) on Metabolism
Insulin resistance (IR) can have numerous metabolic consequences, impacting various aspects of the body's functioning. It can influence glucose disposal rates, hypertension, hyperglycemia, inflammation, visceral adiposity, and endothelial dysfunction (Freeman and Pennings, 2020). The development of IR can be attributed to both genetic and acquired factors. Genetic factors encompass conditions like ataxia-telangiectasia, Werner's syndrome, myotonic dystrophy, Alstr繹m syndrome, Rabson-Mendenhall syndrome, and lipodystrophy. Acquired factors include aging, nutritional imbalances, excess adipose tissue, glucose toxicity, and lipotoxicity. Additionally, certain medications such as protease inhibitors, glucocorticoids, and atypical antipsychotics have been associated with acquired IR (Freeman and Pennings, 2020). If left untreated, IR has the potential to progress to Type 2 Diabetes Mellitus (T2DM).
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