In summary, an imbalance between energy intake and energy expenditure can explain approximately 80% of the variance in body weight gain in this dietary model of obesity. Several metabolic variables appear to contribute to differences in energy balance. A high RQ and an inappropriate suppression of glucose production by insulin appear to be linked to the increase in energy intake that occurs when obesity-prone rats are provided with the high-fat diet. In addition, early tissue enzymatic differences in obesity-prone versus obesity-resistant rats may contribute to differences in energy expenditure and/or to differences in nutrient partitioning. In this dietary model, susceptibility to dietary obesity involves a metabolic environment that includes a high RQ and a reduced ability of insulin to suppress glucose appearance (FIG. 9). However, this environment does not lead to obesity nor to a measurable difference in body weight gain when the susceptible rats are eating a low-fat diet. The high-fat diet is a necessary catalyst for the observed variability in body weight gain and the development of obesity. As a catalyst, the high-fat diet results in an imbalance between energy intake and energy expenditure in some, but not all, rats. This imbalance interacts with the permissive metabolic environment (tissue enzymatic profile favoring carbohydrate utilization and lipid storage) to produce obesity on the high-fat diet. Later, in the HFD feeding period, the rate of weight gain is not significantly different between OP and OR rats, although net fat accumulation remains greater in the former group. It is interesting that this later period is characterized by a reduction in the difference in both RQ and energy intake between OP and OR rats. Thus, during the later stages of HFD feeding, the discrepancy in both energy balance and nutrient balance between OP and OR rats is reduced. This dietary model of obesity is relevant to human obesity. While the prevalence of obesity is high, the majority of people are not obese. The high prevalence of obesity may be due to environmental catalysts that interact with inherent behavioral and metabolic characteristics that favor nutrient retention. Resistance to obesity can be achieved by avoiding these environmental catalysts, by having inherent characteristics that prevent nutrient retention, or both. Our work suggests that the complete understanding of obesity will require not only the identification and functional significance of the genes that determine the inherent capacity of the behavioral and metabolic systems, but also the role of environmental catalysts in determining where and how these systems operate.
Abstract The purpose of the present study was to compare tissue oxidative capacity, skeletal muscle fatty acid composition, and tissue fuel stores in low‐fat fed (LFD, 12% of energy from corn oil) male Wistar rats, and in high‐fat fed (45% of energy from corn oil) obesity‐prone (OP) and obesity‐resistant (OR) male Wistar rats. Designation of OP and OR rats was based on body weight gain (upper tertile for OP; lower tertile for OR) after 5 weeks on the high‐fat diet. Body weight gain over the 5‐week dietary period was 91 ± 9 g in LFD, 98 ± 4 g in OR, and 158 ± 5 g in OP (p<0. 05 vs. LFD and OR). Energy intake over the 5‐week dietary period was 3099 ± 101 kcal in LFD, 3185 ± 51 kcal in OR, and 3728 ± 45 kcal in OP (p<0. 05 vs. LFD and OR). Maximal citrate synthase activity (μ. mol −1 min −1 ) in the gastrocnemius muscle was not significantly different among groups: 12. 1 ± 2. 4 in LFD, 11. 4 ± 1. 9 in OR and 133 ± 2. 5 in OP rats. Similarly, citrate synthase activity in the heart, 59. 3 ± 7. 2, and liver, 6. 6 ± 0. 4, was also not significantly different among groups. Fatty acid composition of the gastrocnemius muscle was not significantly different among groups. Fasting glycogen levels in the liver, gastrocnemius muscle, and heart were 6. 4 ± 3. 7, 13. 2 ± 2. 3 and 6. 8 ± 1. 9 μmol/g in LFD, 21. 2 ± 5. 1 (p<0. 05 vs. LFD and OP), 10. 4 ± 1. 8 and 5. 9 ± 1. 1 mUmol/g in OR, and 36. 3 ± 4. 8 (p<0. 05 vs. LFD and OR), 10. 2 ± 23 and 53 ± 2. 1 μmol/g in OP rats, respectively. Triglyceride levels were similar among groups in plasma, heart and gastrocnemius muscle, but were significantly (p<0. 05) higher in the liver of OP (15. 5 ± 1. 9 (μmol/g) compared to OR (9. 1 ± 1. 1 μmol/g) and LFD (8. 1 ± 1. 4 μmol/g) rats. These data suggest that susceptibility to dietary obesity, in this rodent model, cannot be explained by differences in tissue oxidative capacity or muscle fatty acid composition.
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