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1 INSERM, U724, Faculté de Médecine, BP 184 F 54505 Vandœuvre-les-Nancy, France 2 Université Henri Poincaré, EA 3453, Systèmes Neuromodulateurs des Comportements Ingestifs Nancy, 54000 Nancy, France
(Correspondence should be addressed to B Beck; Email: bernard.beck{at}nancy.inserm.fr)
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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It is also known that the principal hormonal changes that are associated with each type of dietary macronutrient can have either favorable or adverse effects (Wolever 2003, Johnston et al. 2004, Stern et al. 2004). Development of insulin resistance, and more generally of the metabolic syndrome, have been well studied and the overconsumption of both fats and carbohydrates contributes to this development (Reaven 2005). Diet composition also affects adipose tissue hormones such as leptin (Stricker-Krongrad et al. 1998) and adiponectin (Havel 2004, Kadowaki & Yamauchi 2005). It also modulates gastric hormones involved in feeding regulation like ghrelin (Beck et al. 2002, Erdmann et al. 2003, Greenman et al. 2004, Moesgaard et al. 2004, Sanchez et al. 2004, Lindqvist et al. 2005, Pavlatos et al. 2005).
Corticosterone (CORT), which is another important metabolic hormone that is linked to stress situations, is also sensitive to diet composition (Rabolli & Martin 1977, Devenport et al. 1991). Due to the highly variable diet compositions used in different studies, however, it is often quite difficult to compare the data of published reports. Hence, in our present long-term experiment in rats, we have established conditions in which the contribution of carbohydrates to energy balance is maintained at a constant (55% of total calories) level. We then examined the influence of ingestion of diets with proteins (P) and fats (F) providing different proportions of energy on body weight, feeding, and important metabolic hormones. The relationships between adiposity and these hormones (insulin, adipokines, ghrelin, and CORT) were analyzed.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Sixty male Long–Evans rats body weight (BW) 250–300 g; Centre d'Elevage R Janvier, Le Genest St Isle, France) were used in this experiment. The animals were placed in individual wire cages in an air-conditioned room with an automatic 12 h light/12 h darkness cycle (lights on at 0900 h). They were fed a standard laboratory chow (A 04, UAR-Villemoisson sur Orge, France) ad libitum and had tap water to drink for 1 week. During the habituation period to these conditions, the rats ingested about 63 kcal of chow per day.
Then, the rats were randomly distributed into four groups of 15 rats that were fed diets in which the PF energy ratio was symmetrically varied: a HF (PF 5/40), a ‘control’ (PF 15/30), a low-fat (PF 30/15), or a high-protein (PF 40/5) diet. Therefore, each diet provided 55% of its energy from carbohydrates in the form of two-thirds starch and one-third sucrose. The PF 15/30 diet was named ‘control’ by reference to Recommended Dietary Allowances for Humans. The exact composition of the four diets is shown in Table 1.
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Hormone assays
Blood samples were centrifuged at 4 °C for 20 min and the plasma was distributed in aliquots for the determination of insulin, leptin, adiponectin, CORT, and ghrelin levels. These aliquots were kept at –20 °C until assayed.
Plasma glucose and triglycerides were measured by kits using enzymatic methods (BioMérieux, Marcy l'Etoile, France). The hormone levels were measured in duplicate in each case by specific radioimmunoassays using commercially available kits: insulin antibody-coated tubes for immunoreactive insulin (IRI) measurements (Insulin-CT; Cis bio International, Saclay, France) with rat insulin as standard (NOVO, Copenhagen, Denmark), a rat ghrelin kit (RK-031-31; Phoenix Europe GmbH, Karlsruhe, Germany), a rat CORT kit (ICN Pharmaceuticals, Costa Mesa, CA, USA), and a rat leptin kit (RL-83 K; Linco, St Charles, MO, USA). Plasma samples were diluted for the ghrelin assay.
Calculation and statistics
Different indices were calculated: a food efficiency index was calculated as body weight gain during the experiment (in grams) divided by total food intake in grams or kcal; an adipogenicity index was calculated as weight of the three sampled fat depots divided by total food intake in grams or kcal; an insulin sensitivity index was calculated as plasma glucose (mmol/l) divided by plasma insulin (ng/ml). Results are given as the mean±S.E.M. and were compared through variance analysis for repeated measures and/or covariance analysis followed by a post hoc protected least significant difference (PLSD) Fisher's test. Energy intake was the covariant when examining the effects of diet type on hormone profile, insulin sensitivity, and adiposity. Regression curves between hormones and either the adiposity or P/F ratios were also calculated. A probability of 0.05 was considered statistically significant.
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Results |
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There was no difference between the four groups in the chow intake during the habituation period. Energy intake variations during the experiment are shown in Fig. 1. Food intake in the four groups followed parallel variations during the experiment and there were significant effects of both diet and time (P<0.001 for both). In the four groups, energy intake was elevated during week 1 and was stable from week 2 until the end of the experiment. During week 1, energy intake was 21–23% greater than the average intake during the following weeks in the PF 5/40, PF 15/30, and PF 30/15 groups (P<0.001) and 17% greater in the PF 40/5 group (P<0.001). However, there was a clear separation into two subgroups: one comprising the PF 5/40 and the PF 15/30 rats and the other consisting of the PF 30/15 and the PF 40/5 rats. Both PF 30/15 and PF 40/5 rats ingested significantly less energy than the two other groups (cf. Fig. 1) and over the course of the entire experiment, this reduction amounted to about 15% versus PF 15/30 (P<0.001) and about 12% versus PF 5/40 (P<0.001).
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Plasma parameters and hormone profiles
Plasma glucose and triacylglycerol (TG) levels are shown in Table 2. We found a significant effect of diet type on each parameter (P<0.005 for plasma glucose and P<0.001 for triglycerides). Plasma glucose levels were not different between PF 5/40 and PF 15/30 rats, but PF 30/15 and PF 40/5 rats had significantly lower plasma glucose concentrations than the PF 5/40 and PF 15/30 groups (P<0.05; cf. Fig. 4). PF 5/40 rats had significantly higher TG concentrations than the three other groups (P<0.005).
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Adipocytokines (leptin and adiponectin), CORT, and ghrelin concentrations are shown in Fig. 4. All four were also influenced by diet type (P<0.0025 for leptin, P<0.01 for ghrelin, P<0.002 for CORT, and P<0.001 for adiponectin). Leptin levels in PF 5/40 rats were significantly higher than that in the three other groups. Leptin production per unit total adipose tissue was significantly higher in PF 5/40 rats than that in the three other groups (0.77±0.09 versus 0.60±0.11 (PF 15/30), 0.64±0.10 (PF 30/15), 0.66±0.03 (PF 40/5); P<0.025). Ghrelin concentration in the PF 30/15 group was significantly higher than in the three other groups (P<0.001 versus PF 5/40; P<0.05 versus PF 15/30 and PF 40/5).
Adiponectin levels were significantly higher in PF 5/40 rats than that in either PF 15/30 (+25%; P<0.001), PF 30/15 (+40%; P<0.001), or PF 40/5 rats (+47%; P<0.001). In PF 15/30 rats, adiponectin level was higher than that in PF 40/5 rats (+16%; P<0.04). CORT concentrations were significantly higher (2- to 2.5-fold) in PF 40/5 rats than that in the three other groups (P<0.001 versus PF 5/40; P<0.01 versus PF 15/30 and P<0.001 versus PF 30/15).
Relationships between hormone levels, adiposity, and diet composition
Regression curves between the different hormones under study and the fat depot weights as an index of adiposity are shown in Fig. 5. There was a strong correlation found between leptin levels and both adiposity (r=0.79; P<0.0001) and final body weight (r=0.69; P<0.0001) as well as between leptin production per unit deep abdominal adipose tissue (epididymal+perirenal) and final body weight (r=0.28; P=0.03). A significant correlation was also observed between adiposity and on the one hand IRI (r=0.54; P<0.0001) and on the other hand adiponectin (r=0.47; P<0.001). In the case of ghrelin, there was a tendency for an inverse correlation (P<0.08) with adiposity when calculated for the four groups. This correlation became significant when calculated for the PF 5/40, PF 15/30, and PF 30/15 rats only (r=–0.39; P<0.01).
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Discussion |
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The increased palatability of the four diets versus chow, possibly due at least to the presence of sucrose, likely explains the intake of the four groups during week 1 of the experiment. Nonetheless, the rats ingesting the two protein-rich diets ate less than the two other groups. From week 2, there was a metabolic adaptation to these new diets but the clear dichotomy in energy intake between the PF 40/5 and PF 30/15 groups on one hand and the PF 15/30 and PF 5/40 groups on the other hand remained. The two former groups with the highest level of protein went on to consistently eat less than either the PF 15/30 or PF 5/40 rats. A similar reduction in energy intake has been observed in human when the protein content of the diet is increased (Skov et al. 1999, Due et al. 2004, Weigle et al. 2005). The change of diet palatability due to the higher fat content and to the slightly higher sweetness of the PF 15/30 and PF 5/40 diets could also explain the difference in energy intake with the PF 30/15 and the PF 40/5 rats. All four groups of animals in this study regularly gained weight during the course of the experiment but the PF 40/5 rats gained less weight than the three other groups. Food efficiency in the PF 40/5 rats expressed per calorie ingested was not significantly different and the effect on body weight can therefore be attributed to the lower intake of this group. Changes in intake had much more clear-cut impact upon adiposity levels as a marked reduction in deep abdominal adipose tissue mass was observed in PF 30/15 rats and PF 40/5 rats. A lower effect was also observed for the subcutaneous abdominal adipose tissue. These results confirm previous observations of the effects of high-protein diets on visceral adiposity in human or rats (Due et al. 2004, Lacroix et al. 2004). The differences between PF 30/15 or PF 40/5 rats and the two other groups are also likely to be due to some changes in energy expenditure as thermogenesis is increased by a high-protein diet (Johnston et al. 2002, Halton & Hu 2004).
The data from our PF 5/40 rats show that the 10% increase in diet fat content to the detriment of the protein level did not induce any significant change in energy intake when compared with the control rats. This indicates that under conditions of normal carbohydrate availability, rats can rapidly adapt their intake to such relevant changes in the diet composition and control their body weight in a satisfactory manner.
A specific hormonal profile was attached to the phenotype of each dietary group. PF 40/5 and PF 5/40 rats were particularly representative of this phenomenon. In our experiment, PF 40/5 rats had the lowest leptin levels. This is consistent with their lowest adiposity. They differed from the other groups in two respects, their ghrelin and CORT levels. When ghrelin is chronically injected either in the brain or in the periphery, it stimulates food intake and decreases energy expenditure leading to overweight development (Tschop et al. 2000). This hormone is also sensitive to the fat and carbohydrate content of the diet (Beck et al. 2002). Accordingly, we found an inverse correlation between the fat content of the diet and the plasma ghrelin concentrations in the PF 5/40, PF 15/30, and PF 30/15 groups that confirmed some of our previous observations (Beck et al. 2002). The correlation between ghrelin levels and the dietary fat content was no longer evident when the PF 40/5 rats were included in the calculations, thus suggesting that the regulation by ghrelin is either no more functional or less operational when a very low-fat/high-protein content is present in the diet. The threshold is for a P/F ratio >2. This is in agreement with the persistence of ghrelin at levels that are lower than the baseline for a longer duration following a high-protein (45%) meal (AlAwar et al. 2005).
In the PF 40/5 rats, the absence of a further augmentation in ghrelin concentrations is likely to be partly due to their high CORT levels. Ghrelin concentration is indeed lower after a prednisolone treatment or exhibits a strong inverse temporal association with serum cortisol in normal subjects (Otto et al. 2004, Espelund et al. 2005). The CORT increase might also contribute cooperatively with ghrelin to some replenishment of energy stores through their combined action in adipose tissue (Tung et al. 2004). So, the PF 40/5 rats might be more susceptible to weight regain after a dietary change by stimulating fat intake through their high CORT status (Bligh et al. 1990, 1993, Prasad et al. 1995). Additionally, CORT increase is also a sign of activation of the hypothalamo–pituitary axis (HPA). The HPA activation is partly dependent on the macronutrient composition of the diet (Rabolli & Martin 1977, Devenport et al. 1991). For basal CORT, we did not measure any difference between the PF 5/40 and either PF 15/30 or PF 30/15 rats. These data agree with previous experiments showing the absence of variations in basal CORT levels after exposure to a HF diet (Rabolli & Martin 1977, Kamara et al. 1998, Legendre & Harris 2006). However, we cannot exclude a change in sensitivity to stress in the PF 5/40 rats as HF diets augment HPA responsivity to restraint stress with an impact that may vary with the duration of exposure to a HF content (Tannenbaum et al. 1997, Kamara et al. 1998, Legendre & Harris 2006). On the other hand, the presence of sucrose in the diets could have counteracting effects as sucrose or palatable diet ingestion induces a decrease in CORT response to restraint (Strack et al. 1997, Pecoraro et al. 2004) but as HF content, does not alter basal CORT. The high basal CORT measured in the PF 40/5 rats was rather unexpected even if a CORT increase has been observed after a high-protein meal (Gibson et al. 1999). This large increase constitutes a sign of alteration of the HPA axis in the PF 40/5 rats. It is therefore possible that these rats will react differently than the other groups to environmental cues that are either related to nutrition or to other behaviors (e.g., fear, aggressiveness, etc). This is supported, for example, by a greater activity/reactivity of the PF 40/5 rats when opening the cage door for feeding them (personal and non-quantified observations). Ghrelin might contribute to this situation through its anxiogenic effects (Carlini et al. 2002). However, only the measurement of other components of the HPA axis such as central corticotropin-releasing factor in association with different behavioral tests will allow us to confirm this hypothesis in the future.
Our PF 5/40 rats showed the highest levels of leptin that may have served to regulate their food intake near control levels. Their leptin production by unit adipose tissue was also higher and positively associated with final body weight. This confirms several previous findings showing that the leptin system is very sensitive to the fat content of the diet (Ahren et al. 1997, Cooling et al. 1998, Stricker-Krongrad et al. 1998) but not those of Ainslie and colleagues who have shown a negative association between leptin production and body weight in rats fed a moderately HF diet (Ainslie et al. 2000). Diet type and/or rat strain might explain these differences.
The adiponectin levels were paradoxically elevated in the PF 5/40 rats as in rodents; HF diet is associated with insulin resistance and decreased adiponectin (Yamauchi et al. 2001). Our data, however, agree with previous findings in humans showing a positive association between adiponectin and total fat intake (Pischon et al. 2005) and similar variations of adiponectin with the PF ratio have been noted in a recent paper (Morens et al. 2005). This indicates therefore an adaptation to maintain a normal insulin action. This is confirmed by the absence of difference in the insulin sensitivity index that we calculated but the absence of insulin resistance needs, however, to be confirmed by glucose tolerance tests. Maintenance of adequate adiponectin concentration might be related to the low ghrelin levels in PF 5/40 rats. Adiponectin gene expression in adipocytes, which is correlated with plasma levels (DegawaYamauchi et al. 2005), is indeed impaired by chronic exposure to ghrelin (Ott et al. 2002). With a PF ratio of <2, ghrelin appeared to be metabolically active and its lower levels might also help to limit energy intake in PF 5/40 rats. The only adverse dietary effect that we noted in PF 5/40 rats concerned the high concentration of plasma triglycerides that may augment the risk of cardiovascular diseases.
Between the two groups with extreme P/F ratios, variations in ghrelin concentration in the PF 15/30 and PF 30/15 rats indicate that regulatory mechanisms are functioning in a proper manner in these animals to control fat deposits in PF 15/30 rats and stimulate fat storage in PF 30/15 rats at least through ghrelin. A similar increase in ghrelin secretion has been observed in human and rats when fats were substituted for protein in a way similar to our PF 30/15 rats (VallejoCremades et al. 2004, Weigle et al. 2005). Ghrelin levels, however, are unchanged under dietary conditions in which carbohydrates are substituted for fat and when the protein content is unchanged, e.g., when the diet is switched from 35% fat/45% carbohydrates/20% proteins to 15% fat/65% carbohydrates/20% proteins (Weigle et al. 2003). This is also the case when the switch is between protein and fat at a lower (37%) level of carbohydrates (Moran et al. 2005). All these observations indicate that each macronutrient plays an important role for ghrelin regulation.
In conclusion, we show from our current experiments that the PF 40/5 diet comprising a normal supply of energy from carbohydrates was the less obesogenic diet of the four diets that were tested in this study. It was, however, the sole diet that we found could be associated with some signs of HPA activation which might have negative effects in the long term. Quite similar positive effects on adiposity were obtained with the PF 30/15 diet which is less extreme in its macronutrient composition. It is interesting to note that in the conditions we used no obvious signs of insulin resistance were observed. Hence, it will now be interesting to combine these diets with some energy restriction in order to assess whether the same type of regulation occurs and whether differences in body weight loss can be obtained in selected obese subjects.
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Acknowledgements |
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References |
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Received in final form 12 October 2007
Accepted 16 October 2007
Made available online as an Accepted Preprint 16 October 2007
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