Abstract
Caloric restriction, among other behavioral interventions, has demonstrated benefits on improving glycemic control in obesity-associated diabetic subjects. However, an acute and severe intervention without proper maintenance could reverse the initial benefits, with additional metabolic derangements. To assess the effects of an acute caloric restriction in a metabolic syndrome model, a cohort of 15-week old Long Evans Tokushima Otsuka (LETO) and Otsuka Long Evans Tokushima Fatty (OLETF) rats were calorie restricted (CR: 50% × 10 days) with or without a 10-day body mass (BM) recovery period, along with their respective ad libitum controls. An oral glucose tolerance test (oGTT) was performed after CR and BM recovery. Both strains had higher rates of mass gain during recovery vs. ad lib controls; however, the regain was partial (ca. 50% of ad lib controls) over the measurement period. Retroperitoneal and epididymal adipose masses decreased 30% (8.8 g, P < 0.001) in OLETF; however, this loss only accounted for 11.5% of the total BM loss. CR decreased blood glucose AUC 16% in LETO and 19% in OLETF, without significant decreases in insulin. Following CR, hepatic expression of the gluconeogenic enzyme, PEPCK, was reduced 55% in OLETF compared to LETO, and plasma triglycerides (TG) decreased 86%. Acute CR induced improvements in glucose tolerance and TG suggestive of improvements in metabolism; however, partial recovery of BM following CR abolished the improvement in glucose tolerance. The present study highlights the importance of proper maintenance of BM after CR as only partial recovery of the lost BM reversed benefits of the initial mass loss.
Highlights
Obesity and its associated metabolic disorders are significant health problems that have sustained global attention and concern for over the past 3 decades, with an alarming, increasing trend [1, 2]
Obesity is related to 300,000 deaths per year in the United States alone [3], most of them attributed to class II/III obesity (3.8% excess deaths for females, 2.5% males compared to a cohort with normal BMI) [4] and type 2 diabetes mellitus (T2DM) was the underlying cause of death of 75,486 adults in the U.S in 2013 [5]
body mass (BM) gain and food intake were consistently higher in Otsuka Long Evans Tokushima Fatty (OLETF) compared to Long Evans Tokushima Otsuka (LETO), which is consistent for this model of dietinduced obesity [24, 25]
Summary
Obesity and its associated metabolic disorders are significant health problems that have sustained global attention and concern for over the past 3 decades, with an alarming, increasing trend [1, 2]. Excess body mass (BM) and obesity increase morbidity and mortality associated with numerous complications, including T2DM, dyslipidemia, hypertension, and atherosclerosis [6, 7]. Behavioral interventions such as a low-carbohydrate diet [8], caloric restriction (CR) [9], vigorous physical activity (PA), or some combination [10] have demonstrated benefits for improving glycemic control and adiposity in obesity-associated diabetic subjects. Rapid loss of BM can be associated with adipose mass regain and an increase of HOMA-IR over time if vigorous PA or CR is not maintained [11]. The metabolic adjustments associated with CR during metabolic syndrome and following a subsequent regain in BM are not well-elucidated
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