Nutrition has marked influences on gene expression and an understanding of the interaction between nutrients and gene expression is important in order to provide a basis for determining the nutritional requirements on an individual basis. The effects of nutrition can be exerted at many stages between transcription of the genetic sequence and production of a functional protein. This review focuses on the role of post-transcriptional control, particularly mRNA stability, translation and localization, in the interactions of nutrients with gene expression. The effects of both macronutrients and micronutrients on regulation of gene expression by post-transcriptional mechanisms are presented and the post-transcriptional regulation of specific genes of nutritional relevance (glucose transporters, transferrin, selenoenzymes, metallothionein, lipoproteins) is described in detail. The function of the regulatory signals in the untranslated regions of the mRNA is highlighted in relation to control of mRNA stability, translation and localization and the importance of these mRNA regions to regulation by nutrients is illustrated by reference to specific examples. The localization of mRNA by signals in the untranslated regions and its function in the spatial organization of protein synthesis is described; the potential of such mechanisms to play a key part in nutrient channelling and metabolic compartmentation is discussed. It is concluded that nutrients can influence gene expression through control of the regulatory signals in these untranslated regions and that the post-transcriptional regulation of gene expression by these mechanisms may influence nutritional requirements. It is emphasized that in studies of nutritional control of gene expression it is important not to focus only on regulation through gene promoters but also to consider the possibility of post-transcriptional control.

The main role of diet is to provide enough nutrients to meet the requirements of a balanced diet, while giving the consumer a feeling of satisfaction and well-being. The most recent knowledge in bioscience supports the hypothesis that diet also controls and modulates various functions in the body, and, in doing so, contributes to the state of good health necessary to reduce the risk of some diseases. It is such an hypothesis which is at the origin both of the concept of ‘functional food’ and the development of a new scientific discipline of ‘functional food science’. In the context of this paper the potential ‘functional foods’ to be discussed are the prebiotics and the synbiotics. The prebiotics developed so far are the non-digestible oligosaccharides and especially the non-digestible fructans among which chicory fructans play a major role. The chicory fructans are β (2-1) fructo-oligosaccharides classified as natural food ingredients. They positively affect various physiological functions in such a way that they are already or may, in the future, be classified as functional food ingredients for which claims of functional effects or of disease risk reduction might become authorized. They are classified as prebiotic and have been shown to induce an increase in the number of bifidobacteria in human faecal flora. As part of a synbiotic-type product, they are already bifidogenic at a dose of 2·75 g/d and the effect lasts for at least 7 weeks. The other potential functional effects are on the bioavailability of minerals, but also, and more systemically, on the metabolism of lipids. Potential health benefits may concern reduction of the risk of intestinal infectious diseases, cardiovascular disease, non-insulin-dependent diabetes, obesity, osteoporosis and cancer. However, except for the prebiotic effect, and tentatively the improvement of calcium bioavailability, the evidence to support such effects is still missing in humans though hypotheses already exist to justify nutrition studies.

Previous studies in this laboratory have elicited a monophasic response in postprandial plasma triacylglycerol (TAG) level with fat intakes of 0.5 g fat/kg body weight accompanied by about 17 g carbohydrate as lactose. Recent studies involving the same level of fat with a higher level of carbohydrate, 136 g of which 60 g was sucrose, appeared to elicit a biphasic response. The present study compared these two test meals and showed a significant meal × time interaction for plasma total TAG (P = 0.0228) reflecting a monophasic response with the lower-carbohydrate test meal. The higher-carbohydrate meal induced significantly higher insulin and glucose-dependent insulinotropic polypeptide responses (P = 0.0009 and P = 0.0041 respectively). A significant meal × time interaction was seen for plasma non-esterified fatty acids (P = 0.0437). The biphasic plasma TAG response seen with the high-carbohydrate meal largely reflected the TAG-rich lipoprotein (TRL) or chylomicron fraction, which would tend to suggest a biphasic pattern of absorption. This was borne out by TRL-TAG fatty acid compositions. Both peaks in the biphasic response showed active incorporation of the main dietary fatty acids, 18:1n−9, 18:2n−6 and 18:3n−3 into TRL-TAG. These results indicate that under the specific test-meal conditions used in the present study, a biphasic pattern of fat absorption was seen.

Lipoprotein lipase (EC 3.1.1.34; LPL) is a key enzyme regulating the disposal of lipid fuels in the body. It is expressed in a number of peripheral tissues including adipose tissue, skeletal and cardiac muscle and mammary gland. Its role is to hydrolyse triacylglycerol (TG) circulating in the TG-rich lipoprotein particles in order to deliver fatty acids to the tissue. It appears to act preferentially on chylomicron-TG, and therefore may play a particularly important role in regulating the disposition of dietary fatty acids. LPL activity is regulated according to nutritional state in a tissue-specific manner according to the needs of the tissue for fatty acids. For instance, it is highly active in lactating mammary gland; in white adipose tissue it is activated in the fed state and suppressed during fasting, whereas the reverse is true in muscle. Such observations have led to the view of LPL as a metabolic gatekeeper, especially for dietary fatty acids. However, closer inspection of its action in white adipose tissue reveals that this picture is only partially true. Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow. LPL appears to act as one member of a series of metabolic steps which are regulated in a highly coordinated manner. In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL. This involves regulation of the pathway of fatty acid uptake and esterification, and appears to be regulated by a number of factors including insulin, acylation-stimulating protein and possibly leptin.

Raised plasma triacylglycerol is an independent risk factor for cardiovascular disease, and an understanding of factors which regulate the synthesis and degradation of lipoproteins which carry triacylglycerol in the blood may lead to novel approaches to the treatment of hypertriacylglycerolaemia. An active microsomal triacylglycerol transfer protein (MTP) is essential for the assembly of particles which transport triacylglycerol through the circulation. After absorption in the intestine, dietary fat and fat-soluble vitamins are incorporated into chylomicrons in the intestinal epithelial cells, and these lipoproteins reach the bloodstream via the lymphatic system. Patients with the rare genetic disorder, abetalipoproteinaemia, in which MTP activity is absent, present clinically with fat-soluble vitamin and essential fatty acid deficiency, indicating a key role for MTP in the movement of fat into the body. The triacylglycerol-rich lipoprotein found in fasting blood, VLDL, is assembled in the liver by an MTP-dependent process similar to chylomicron assembly, and transports triacylglycerol to extra-hepatic tissues such as adipose tissue and heart. In the absence of MTP activity, VLDL are not synthesized and only extremely low levels of triacylglycerol are present in the blood. Dietary components, including fat, cholesterol and ethanol, can modify the expression of the MTP gene and, hence, MTP activity. The present review summarizes current knowledge of the role of MTP in the assembly and secretion of triacylglycerol-rich lipoproteins, and the regulation of its activity in both animal and cell systems.

The effects of dietary red pepper added to high-fat (HF) and high-carbohydrate (HC) meals on energy metabolism were examined in thirteen Japanese female subjects. After ingesting a standardized dinner on the previous evening, the subjects took an experimental breakfast (1883 kJ) under the following four conditions: HF meal, HF and red-pepper (10 g) meal, HC meal, or HC and red-pepper meal. Palatability of the experimental meals was measured immediately after the meals. Expired air was collected before and for 210 min after the meal to determine energy expenditure and macronutrient oxidation. Diet-induced thermogenesis was significantly higher after the HC meals than after the HF meals. Lipid oxidation was significantly lower and carbohydrate oxidation was significantly higher after the HC meals than after the HF meals. Addition of red pepper to the experimental meals significantly increased diet-induced thermogenesis and lipid oxidation, particularly after the HF meal. On the other hand, carbohydrate oxidation was significantly decreased by the addition of red pepper to the experimental meals. Addition of red pepper to the HC meal increased the perceived oiliness of the meal to the same level as that of the HF meals. These results indicate that red pepper increases diet-induced thermogenesis and lipid oxidation. This increase in lipid oxidation is mainly observed when foods have a HF content whereas the increase in the perceived oiliness of the meal was found under the HC meal conditions.

This study reports results from a randomized controlled intervention trial, focusing on: (1) the identification of successful consumer strategies for increasing fruit and vegetable intakes to the recommended levels of more than five (80 g) portions per day and (2) impact on overall diet and nutrient intakes. Adult men and women (n 170) fulfilling the main recruitment criterion of eating less than five fruit and vegetable portions per day but contemplating increasing intakes were recruited. Complete valid dietary data was provided by 101 intervention (fifty-nine estimated fruit and vegetable intakes, and forty-two simultaneous weighed total dietary and estimated fruit and vegetable intakes) and twenty-four control subjects (weighed total dietary intakes). Intervention advice included the specific association of high fruit and vegetable intake with reduced risk of disease, practicalities, and portion definition with a target intake of greater than five 80 g fruit and vegetable portions per day for 8 weeks. There were significant effects (P < 0·001) on weighed intakes of fruit and vegetables in the intervention group, rising from 324 (se 25) to 557 (se 31) g/d and reflected by validated portion measures at 8 weeks intervention. Successful strategies chosen by ‘achievers’ of the target intake (65% of subjects) were conventional (fruit as a snack, vegetables with main meals etc.) and favoured fruit. There were significant increases in percentage energy from carbohydrate (from sugars not starch), vitamin C, carotenes and NSP and there was a significant decrease in percentage energy from fat for subjects who had high fat intakes (> 35% energy) at baseline. Follow-up self-reported measures at 6 and 12 months indicated mean intakes of 4·5 and 4·6 defined portions/d respectively, suggesting some sustainable effect. In conclusion, the intervention led to significant increases in fruit and vegetable intakes largely via conventional eating habits, with some desirable effects on macro- and micronutrient intakes.