Bacterial Methionine Metabolism Genes Influence Drosophila melanogaster Starvation Resistance.

Animal-associated microorganisms (microbiota) dramatically influence the nutritional and physiological traits of their hosts. To expand our understanding of such influences, we predicted bacterial genes that influence a quantitative animal trait by a comparative genomic approach, and we extended these predictions via mutant analysis. We focused on Drosophila melanogaster starvation resistance (SR). We first confirmed that D. melanogaster SR responds to the microbiota by demonstrating that bacterium-free flies have greater SR than flies bearing a standard 5-species microbial community, and we extended this analysis by revealing the species-specific influences of 38 genome-sequenced bacterial species on D. melanogaster SR. A subsequent metagenome-wide association analysis predicted bacterial genes with potential influence on D. melanogaster SR, among which were significant enrichments in bacterial genes for the metabolism of sulfur-containing amino acids and B vitamins. Dietary supplementation experiments established that the addition of methionine, but not B vitamins, to the diets significantly lowered D. melanogaster SR in a way that was additive, but not interactive, with the microbiota. A direct role for bacterial methionine metabolism genes in D. melanogaster SR was subsequently confirmed by analysis of flies that were reared individually with distinct methionine cycle Escherichia coli mutants. The correlated responses of D. melanogaster SR to bacterial methionine metabolism mutants and dietary modification are consistent with the established finding that bacteria can influence fly phenotypes through dietary modification, although we do not provide explicit evidence of this conclusion. Taken together, this work reveals that D. melanogaster SR is a microbiota-responsive trait, and specific bacterial genes underlie these influences.IMPORTANCE Extending descriptive studies of animal-associated microorganisms (microbiota) to define causal mechanistic bases for their influence on animal traits is an emerging imperative. In this study, we reveal that D. melanogaster starvation resistance (SR), a model quantitative trait in animal genetics, responds to the presence and identity of the microbiota. Using a predictive analysis, we reveal that the amino acid methionine has a key influence on D. melanogaster SR and show that bacterial methionine metabolism mutants alter normal patterns of SR in flies bearing the bacteria. Our data further suggest that these effects are additive, and we propose the untested hypothesis that, similar to bacterial effects on fruit fly triacylglyceride deposition, the bacterial influence may be through dietary modification. Together, these findings expand our understanding of the bacterial genetic basis for influence on a nutritionally relevant trait of a model animal host.

Deciphering a neuronal circuit that mediates appetite.

Hypothalamic neurons that co-express agouti-related protein (AgRP), neuropeptide Y and γ-aminobutyric acid (GABA) are known to promote feeding and weight gain by integration of various nutritional, hormonal, and neuronal signals. Ablation of these neurons in mice leads to cessation of feeding that is accompanied by activation of Fos in most regions where they project. Previous experiments have indicated that the ensuing starvation is due to aberrant activation of the parabrachial nucleus (PBN) and it could be prevented by facilitating GABA(A) receptor signalling in the PBN within a critical adaptation period. We speculated that loss of GABA signalling from AgRP-expressing neurons (AgRP neurons) within the PBN results in unopposed excitation of the PBN, which in turn inhibits feeding. However, the source of the excitatory inputs to the PBN was unknown. Here we show that glutamatergic neurons in the nucleus tractus solitarius (NTS) and caudal serotonergic neurons control the excitability of PBN neurons and inhibit feeding. Blockade of serotonin (5-HT(3)) receptor signalling in the NTS by either the chronic administration of ondansetron or the genetic inactivation of Tph2 in caudal serotonergic neurons that project to the NTS protects against starvation when AgRP neurons are ablated. Likewise, genetic inactivation of glutamatergic signalling by the NTS onto N-methyl D-aspartate-type glutamate receptors in the PBN prevents starvation. We also show that suppressing glutamatergic output of the PBN reinstates normal appetite after AgRP neuron ablation, whereas it promotes weight gain without AgRP neuron ablation. Thus we identify the PBN as a hub that integrates signals from several brain regions to bidirectionally modulate feeding and body weight.

S-Carboxyethylcysteine (a constituent of Acacia seed) negatively affects casein protein utilization by rats.

OBJECTIVE: Two rat bioassay experiments are reported. The first investigated the first limiting amino acid in Acacia colei and the second experiment investigated the effect of S-carboxyethylcysteine (CEC; a compound present in acacia seed) on protein use. METHODS: In the first experiment, Wistar rats were fed A. colei seed supplemented with three levels of methionine, cysteine, and tryptophan (0.1%, 0.2%, and 0.4%). In the second experiment, the Wistar rats were fed CEC-incorporated casein diets. RESULTS: Supplementation of A. colei with tryptophan had no significant effect on the protein efficiency ratio, cysteine showed the highest protein efficiency ratio value at the 0.4% level, and the protein efficiency ratio increased significantly with the increase in methionine content, making methionine the first limiting amino acid. The methionine-induced growth rate was suppressed by the incorporation of CEC, which also had a negative effect on the plasma amino acid levels. CONCLUSION: The results indicated that methionine is the first limiting amino acid in A. colei and that CEC could affect the seed's protein use. Acacia colei seed can be used effectively as famine food only if it is complemented with other cereals known to be rich in sulfur amino acids.

Nutritional enhancement of US Title II food aid products.

BACKGROUND: Food aid provided by the United States has saved the lives of the vulnerable for many years. Recognizing the need for a thorough review of product formulations and specifications, the US Agency for International Development (USAID) commissioned a 2-year assessment of quality issues relating to Title II food aid products. This article presents findings and recommendations of that review relating to product enhancements. OBJECTIVE: The core question addressed was: Are current commodity specifications for enriched FBFs appropriate in light of evolving nutritional science and food fortification technology, or do they need to be updated? METHODS: Empirical data were derived from a number of sources, including a survey of Title II implementing partners focusing on procurement and logistics, and uses of FBFs and other foods. Input of implementing partners, civil society, and donor organizations was obtained through individual consultations, international and small group meetings. More than 400 individuals accessed the project's website. The project convened a panel of experts in food technology and science, food policy, law, industry, medicine, development and humanitarian work, and the maritime industry, and held regular joint meetings with USDA and USAID. The draft report was widely disseminated and posted on the website. RESULTS AND CONCLUSIONS: The findings of this research led to the following broad areas of improvement in US Title II food aid products: 1) Improve the formulation of existing FBF products used in Title II programming. This includes the addition of a dairy source of protein to products targeted to children 6 to 24 months of age, pregnant and lactating women, wasted children, and wasted individuals undergoing HIV/AIDS treatment. 2) Upgrade the vitamin and mineral mixes used and diversify approaches to addressing micronutrient needs. Enhance the composition of premixes used to fortify blended foods as well as milled grains and vegetable oil; facilitate shipping offortificant premix with bulk cereals for in-country fortification; and develop micronutrient powders (sachets) and other point-of-use fortification options. 3) Develop or adopt non-cereal-based (e.g., lipid-based) products for the management of nutritional deficiencies. This is an argument for more choice among appropriate tools, not for discarding products that have already shown their value over many years. It also does not reduce the need to maintain a focus on supplying high volumes of quality grains as the main staple in food aid baskets.

Hunger and malnutrition: the determinant of development: the case for Africa and its food and nutrition workers.

Hunger and malnutrition in Africa have been on the increase since 1960's reaching a climax in the 1980's when over 150 million people were affected by one form or another. Methods so far used to solve the problem do not seem to succeed, but the scientists and leaders in Africa could now take the opportunity to consider and act on the problem in their own way. The formation of an African food and nutrition group to work with others on the problems, could give an impetus to this kind of initiative. A call is made to all African food and nutrition workers to combine efforts to harness Africa resources, which have not been fully utilized in solving the problem.

PIP: Hunger and malnutrition in Africa have been on the increase since the 1960s. During the 1970s, it is estimated that 30 million people were directly affected by famine and malnutrition. About 5 million children died in 1984 alone. In Mozambique during the 1983-84 famine, about 100,000 people perished. In Ethiopia, Sudan, Somalia, Liberia, and Angola armed conflicts compound the problem. Ethiopia alone had 9 million famine victims in 1983. The most common form of malnutrition in Africa is protein energy deficiency affecting over 100 million people, especially 30-50 million children under 5 years of age. Almost another 200 million are at risk. Iron deficiency, commonly called anemia, also affects 150 million people, mostly women and children. Iodine deficiency leads to disorders like mental retardation, cretinism, deafness, abortion, low resistance to disease, and goiter and this affects 60 million with about 150 million more at risk. Vitamin A deficiency causes blindness and low resistance to disease and affects about 10 million. Protein energy deficiency is treated by using donated foods in hospitals, rehabilitation centers, day care centers, and feeding centers. There are no community programs for anemia, or vitamin A or iodine deficiencies. Vaccines for preventing and drugs for treating diseases that cause malnutrition are imported. Therefore, African food and nutrition professionals met in 1988 and created the Africa Council for Food and Nutrition Sciences (AFRONUS) to eliminate famine and malnutrition in Africa. Activities have started in: 1) developing contacts between the workers in food and nutrition; 2) assessing the situation of food and nutrition in Africa; 3) developing an action plan; 4) implementing the plan; and 5) monitoring progress. Food and Nutrition Policy Guidelines have also been prepared by AFRONUS for food and nutrition workers. Africa has enough natural resources to solve the problem of hunger and malnutrition, but these resources have to be harnessed.

Phosphorus and mankind's problems today.

The unprecedented increase in the worldwide population of humans--a growth which has been underway for two centuries and has been continuously accelerating--seems to be a root cause of many of the problems of today, including including those treated in this symposium. Current events once more arouse fears that the probable conclusion of our present growth era will unfortunately consist of widespread death from famine, pestilence, and social disruption of various kinds (perhaps involving nuclear devices). Non-local efforts to avoid famine induced by rapid population growth seem only to delay an eventuality that will thereby finally lead to many more people starving. In this paper, phosphate pollution and soil erosion are treated as indirect results of the population boom; and some radical changes in soil and water management are suggested for lessening these problems for large populations.