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Glucose Tolerance and Triglyceridemia Improves During Acute Caloric Restriction Without Changes in SBP in Obese, Insulin Resistant Rats
Author(s) -
Cornejo Manuel Alejandro,
Nguyen Julie,
Cazares Joshua,
Escobedo Benny,
Nishiyama Akira,
Ortiz Rudy
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.883.1
Subject(s) - medicine , insulin resistance , endocrinology , lean body mass , weight loss , insulin , blood pressure , obesity , body weight
The recovery of body mass following caloric restriction (CR)‐induced mass loss has been associated with increased plasma triglycerides and insulin resistance index (IRI) in obese humans [1]. Food efficiency (mass gain: caloric intake ratio) increased 142% in diet‐induced obese rats undertaking a series of mass loss‐regain cycles [2]. Moreover, obese humans lose significant lean tissue (about one quarter of total mass lost) during CR, which can be only partially ameliorated by exercise programs (about 10% reduction of the lean: fat tissue reduction loss) [3]. Our goal was to look for deleterious effects in insulin sensitivity, adiposity and lean tissue conservation derived from body mass recovery after CR, in an obese, insulin resistant animal model. Twenty‐eight lean Long Evans Tokushima Otsuka (LETO) rats and 28 obese, insulin resistant Otsuka Long Evans Tokushima Fatty rats (OLETF) were separated in two control groups (n=14 each), two CR groups (n=14 each), and two recovery groups (n=14 each). All groups were fed ad libidum for 4 weeks except the control groups, which were fed ad libidum for 16 weeks. After 4 weeks, CR and recovery groups were fed half the mean food intake of the ad libidum LETO group for 10 days, after which they were subjected to an oral glucose tolerance test (oGTT) and later dissection. After the CR, recovery groups were fed ad libidum for 7 days, subjected to oGTT, and dissected. Mass ( Fig. 1) and food intake were recorded daily. Systolic, diastolic, and mean arterial pressure were measured by tail‐cuff plethysmography daily. Blood glucose and plasma insulin were measured at 0, 15, 30, 60 and 120 min during oGTT. Both AUC for glucose and insulin concentrations were multiplied to obtain the IRI (Fig. 2). Additional measures of lipid and protein metabolism were measured. Mean mass increment per day (calculated as the slope of the linear equation of each group) increased in LETO from 2.55 g/day in control to 5.28 g/day in recovery group, and increased from 3.78 to 6.82 g/day in OLETF. Differences in blood pressure were significant between LETO and OLETF, but not among groups. IRI decreased to roughly half the baseline level after CR in OLETF (19.7 ± 2.4 to 10.6 ± 2.1 relative units) and increased to 18.7 ± 1.9 RU after refeeding, while IRI decreased in LETO (8.3 ± 0.4 to 5.4 ± 0.3 RU after CR). Relative retroperitoneal fat mass in OLETF decreased by 0.7% after CR and did not recover with refeeding. Similarly, relative epididymal fat mass decreased 0.3% and did not recover. Creatinine concentration decreased in OLETF (0.36 ± 0.02 to 0.28 ± 0.06 mg/dl) but increased in LETO rats (0.35 ± 0.02 to 0.54 ± 0.06 mg/dl) in CR groups compared to baseline. Triglycerides concentration decreased in OLETF from 42.2 ± 7.2 to 6.1 ± 1.2 mg/dl after CR, and returned to baseline levels (40.5 ± 7.1 mg/dl) after recovery. In conclusion, IR was ameliorated during CR, but had no profound effect on SBP. Moreover CR resulted in an expected loss of fat mass and concomitant decrease in triglyceride levels, associated with a higher loss of lean mass in OLETF. 1Animal Body Mass (g) by day. Slope was calculated in Control and Recovery groups and reported as mean mass increment per day (not shown).