Control of voluntary feed intake in fish: a role for dietary oxygen demand in Nile tilapia (Oreochromis niloticus) fed diets with different macronutrient profiles

Abstract

It has been hypothesised that, at non-limiting water oxygen conditions, voluntary feed intake (FI) in fish is limited by the maximal physiological capacity of oxygen use (i.e. an 'oxystatic control of FI in fish'). This implies that fish will adjust FI when fed diets differing in oxygen demand, resulting in identical oxygen consumption. Therefore, FI, digestible energy (DE) intake, energy balance and oxygen consumption were monitored at non-limiting water oxygen conditions in Nile tilapia fed diets with contrasting macronutrient composition. Diets were formulated in a 2 £ 2 factorial design in order to create contrasts in oxygen demand: two ratios of digestible protein (DP):DE ('high' v. 'low'); and a contrast in the type of non-protein energy source ('starch' v. 'fat'). Triplicate groups of tilapia were fed each diet twice daily to satiation for 48 d. FI (g DM/kg 0·8 per d) was significantly lower (9·5 %) in tilapia fed the starch diets relative to the fat diets. The DP:DE ratio affected DE intakes (P,0·05), being 11 % lower with 'high' than with 'low' DP:DE ratio diets, which was in line with the 11·9 % higher oxygen demand of these diets. Indeed, DE intakes of fish showed an inverse linear relationship with dietary oxygen demand (DOD; R 2 0·81, P,0·001). As hypothesised ('oxystatic' theory), oxygen consumption of fish was identical among three out of the four diets. Altogether, these results demonstrate the involvement of metabolic oxygen use and DOD in the control of FI in tilapia.Key words: Feed intake: Oxygen consumption: Non-protein energy sources: Energy balance: FishVoluntary feed intake (FI) in fish, as in other animals, is controlled by a complex combination of nutritional, physiological and environmental factors (1) . It has frequently been suggested that FI is controlled to maintain a relatively constant digestible energy (DE) intake, i.e. to meet the DE requirements (2 -6) .However, a few studies in fish have suggested the involvement of other nutritional factors in the control of FI (7,8) . Studies that verify the importance of other well-known regulatory mechanisms of FI in mammals, such as glucostatic (9) or lipostatic control (10) , either lead to an ambiguous conclusion or show a lesser impact in fish (7,11) than in terrestrial animals. The effect of non-protein energy (NPE) source (fat and starch) on FI in fish is unclear (12) and has not been systematically assessed at least at a similar digestible protein (DP):DE ratio and DE content of diets. Among the abiotic factors, dissolved oxygen (DO), pH and NH 3 are recognised to affect FI in fish (13) . The effect of the availability of oxygen on FI has been relatively well documented. Several studies have demonstrated that FI in fish decreases linearly with declining water DO content (14 -17) .The minimum DO level at which metabolic oxygen demand in fish limits FI is termed as incipient DO (iDO). Thus, * Corresponding author: J. W. Schrama, fax þ31 317 483937, email johan.schrama@wur.nlAbbreviations: ADC, apparent digestibility coefficie...

Voluntary Feed Intake in Rainbow Trout Is Regulated by Diet-Induced Differences in Oxygen Use

“…An enhanced oxidative metabolism over the long term has been suggested to impart putative negative effects (e.g., the buildup of reactive oxygen species) on the animal (27,28). In view of the above findings, we previously proposed a role of oxygen consumption in the control of voluntary feed intake in Nile tilapia fed diets highly varying in macronutrient composition (11). In that study, Nile tilapia linearly adjusted the feed intake (DEI) depending on the diet-induced differences in oxygen use and, moreover, had a similar oxygen consumption in some of the diet groups, which suggests that perhaps physiological factors related to oxygen consumption constrained the feed intake.…”

“…It has often been suggested that fish, like other animals, adjust their voluntary feed intake according to the digestible energy content of the diet in order to meet a predefined energy requirement (2)(3)(4). However, recent findings in rainbow trout (5)(6)(7)(8)(9)(10) and other teleosts (6,11,12) contradict the notion that feed intake is adjusted to have a constant digestible energy intake (DEI) 6 . Similarly, the demand for a target lean growth or protein deposition rather than for a predefined energy requirement has been proposed to regulate feed intake in fish (8,10,13,14).…”

“…Similarly, the demand for a target lean growth or protein deposition rather than for a predefined energy requirement has been proposed to regulate feed intake in fish (8,10,13,14). However, several other fish studies did not show an equal protein deposition with satiation feeding (e.g., 7,11). The dietinduced difference in the voluntary intake levels observed in various fish species (7,9,(15)(16)(17) might be related to the type and level of dietary nonprotein digestible energy (NPDE) source (starch vs. fat) as suggested in mammals [for review, see (18).…”

“…In terrestrial animals, dietary starch and fat exert their effects on feed intake via feedback mechanisms mediated by circulating glucose (19) (glucostatic regulation) and body fat store (20) (lipostatic regulation), respectively. These chemostatic control mechanisms of feed intake show inconsistent outcomes in fish (7,11). Alternatively, the thermostatic regulation of feed intake in homeotherms proposes the intake to be controlled by the animalÕs need for body heat and its ability to dissipate the extra heat to the environment generated as a by-product of food processing (21,22).…”

Growth performance of hybrid striped bass (Morone chrysops × M. saxatilis) fed with commercial pike perch and trout diets

“…It is known that excess dietary protein and lipid levels can negatively influence the SGR and FCR in fish (Brown et al 1992;Hatlen et al 2007;Peres and Oliva-Teles 1999;Saravanan et al 2012). Excess dietary lipid increases adiposity, which is thought to exert a negative feedback on feed intake via lipostatic regulation mechanisms (Johansen et al 2002).…”