The African Goat Improvement Network: a scientific group empowering smallholder farmers.

The African Goat Improvement Network (AGIN) is a collaborative group of scientists focused on genetic improvement of goats in small holder communities across the African continent. The group emerged from a series of workshops focused on enhancing goat productivity and sustainability. Discussions began in 2011 at the inaugural workshop held in Nairobi, Kenya. The goals of this diverse group were to: improve indigenous goat production in Africa; characterize existing goat populations and to facilitate germplasm preservation where appropriate; and to genomic approaches to better understand adaptation. The long-term goal was to develop cost-effective strategies to apply genomics to improve productivity of small holder farmers without sacrificing adaptation. Genome-wide information on genetic variation enabled genetic diversity studies, facilitated improved germplasm preservation decisions, and provided information necessary to initiate large scale genetic improvement programs. These improvements were partially implemented through a series of community-based breeding programs that engaged and empowered local small farmers, especially women, to promote sustainability of the production system. As with many international collaborative efforts, the AGIN work serves as a platform for human capacity development. This paper chronicles the evolution of the collaborative approach leading to the current AGIN organization and describes how it builds capacity for sustained research and development long after the initial program funds are gone. It is unique in its effectiveness for simultaneous, multi-level capacity building for researchers, students, farmers and communities, and local and regional government officials. The positive impact of AGIN capacity building has been felt by participants from developing, as well as developed country partners.

Intake of seafood in the US varies by age, income, and education level but not by race-ethnicity.

Current US federal dietary guidance recommends regular consumption of seafood (fish + shellfish) to promote health; however, little is known about how well Americans meet the guideline, particularly population subgroups that may be at risk for inadequate intake. The purposes of this study were to describe the prevalence of seafood consumption and, among consumers, the amounts of seafood eaten by sex, age group, income and education level, and race-ethnicity. Data from 15,407 adults aged 19+ participating in the 2005-2010 National Health and Nutrition Examination Surveys were analyzed using methods to account for sporadic intake of seafood. Over 80% of Americans reported consuming any seafood over the past 30 days, 74% reported consuming fish, and 54% reported eating shellfish. The percentages varied by socio-demographic group. Younger age and lower income and education levels were associated with lower odds of being a seafood consumer (p < 0.0001). Among those who reported eating seafood, the average amount eaten of any seafood was 158.2 ± 5.6 g/week. Among seafood consumers, women and individuals of lower age and education levels consumed less seafood. Approximately 80%-90% of seafood consumers did not meet seafood recommendations when needs were estimated by energy requirements. A great deal of work remains to move Americans toward seafood consumption at current recommended levels.

Issues of fish consumption for cardiovascular disease risk reduction.

Increasing fish consumption is recommended for intake of omega-3 (n-3) fatty acids and to confer benefits for the risk reduction of cardiovascular disease (CVD). Most Americans are not achieving intake levels that comply with current recommendations. It is the goal of this review to provide an overview of the issues affecting this shortfall of intake. Herein we describe the relationship between fish intake and CVD risk reduction as well as the other nutritional contributions of fish to the diet. Currently recommended intake levels are described and estimates of fish consumption at a food disappearance and individual level are reported. Risk and benefit factors influencing the choice to consume fish are outlined. The multiple factors influencing fish availability from global capture and aquaculture are described as are other pertinent issues of fish nutrition, production, sustainability, and consumption patterns. This review highlights some of the work that needs to be carried out to meet the demand for fish and to positively affect intake levels to meet fish intake recommendations for CVD risk reduction.

Insulin-like growth factor-I and genetic effects on indexes of protein degradation in response to feed deprivation in rainbow trout (Oncorhynchus mykiss).

This study determined the effect of genetic variation, feed deprivation, and insulin-like growth factor-I (IGF-I) on weight loss, plasma IGF-I and growth hormone, and indexes of protein degradation in eight full-sibling families of rainbow trout. After 2 wk of feed deprivation, fish treated with IGF-I lost 16% less (P < 0.05) wet weight than untreated fish. Feed deprivation increased growth hormone (P < 0.05) and decreased IGF-I (P < 0.05), but hormone levels were not altered by IGF-I. Plasma 3-methylhistidine concentrations were not affected by IGF-I but were decreased after 2 wk (P < 0.05) and increased after 4 wk (P < 0.05) of feed deprivation. In white muscle, transcript abundance of genes in the ubiquitin-proteasome, lysosomal, and calpain- and caspase-dependent pathways were affected by feed deprivation (P < 0.05). IGF-I prevented the feed deprivation-induced upregulation of MAFbx (F-box) and cathepsin transcripts and reduced abundance of proteasomal mRNAs (P < 0.05), suggesting that reduction of protein degradation via these pathways may be partially responsible for the IGF-I-induced reduction of weight loss. Family variations in gene expression, IGF-I concentrations, and weight loss during fasting suggest genetic variation in the fasting response, with considerable impact on regulation of proteolytic pathways. These data indicate that nutrient availability, IGF-I, and genetic variation affect weight loss, in part through alterations of proteolytic pathways in rainbow trout, and that regulation of genes within these pathways is coordinated in a way that supports a similar physiological response.

Spleen size predicts resistance of rainbow trout to Flavobacterium psychrophilum challenge.

Selective breeding of animals for increased innate resistance offers an attractive strategy to control disease in agriculture. However, this approach is limited by an incomplete knowledge of the heritability, duration, and mechanism(s) of resistance, as well as the impact of selection on the immune response to unrelated pathogens. Herein, as part of a rainbow trout broodstock improvement program, we evaluated factors involved in resistance against a bacterial disease agent, Flavobacterium psychrophilum. In 2005, 71 full-sibling crosses, weighing an average of 2.4 g, were screened, and resistant and susceptible crosses were identified. Naive cohorts were evaluated at 10 and 800 g in size, and most maintained their original relative resistant or susceptible phenotypes, indicating that these traits were stable as size increased >300-fold. During the course of these studies, we observed that the normalized spleen weights of the resistant fish crosses were greater than those of the susceptible fish crosses. To test for direct association, we determined the spleen-somatic index of 103 fish crosses; created high, medium, and low spleen-index groups; and determined survival following challenge with F. psychrophilum or Yersinia ruckeri. Consistent with our previous observations, trout with larger spleen indices were significantly more resistant to F. psychrophilum challenge; however, this result was pathogen-specific, as there was no correlation of spleen size with survival following Y. ruckeri challenge. To our knowledge, this is the first report of a positive association between spleen size and disease resistance in a teleost fish. Further evaluation of spleen index as an indirect measure of disease resistance is warranted.

Suggestive association of major histocompatibility IB genetic markers with resistance to bacterial cold water disease in rainbow trout (Oncorhynchus mykiss).

Genes within the major histocompatibility complex (MHC) are important for both innate and adaptive immune responses in mammals; however, much less is known regarding their contribution in teleost fishes. We examined the involvement of four major histocompatibility (MH) genomic regions in rainbow trout in resistance to the causative agent of bacterial coldwater disease (BCWD), Flavobacterium psychrophilum. Fish from the 2005 NCCCWA brood-year (71 full-sib families) were challenged with F. psychrophilum strain CSF 259-93. The overall mortality rate was 70%, with large variation in mortality between families. Disease resistance was quantified as post-challenge days to death. Phenotypic variation and additive genetic variation were estimated using mixed models of survival analysis. To examine association, eight microsatellite markers were isolated from MH gene-containing BAC clones and mapped onto the rainbow trout genetic linkage map. The parents and grandparents of the 2005 brood-year families were genotyped with these eight markers and another two markers tightly linked to the MH-IB region to assess the extent of linkage disequilibrium (LD) of MH genomic regions MH-IA, MH-IB, TAP1, and MH-II with survival post-challenge. MH-IB and MH-II markers were linked to BCWD survivability when data were analyzed by family. Tests for disease association at the population level substantiated the involvement of MH-IB, but not MH-II, with disease resistance. The impact of selective breeding for disease resistance on MH sequence variation is discussed in the context of aquaculture production.

Effects of short-term growth hormone treatment on liver and muscle transcriptomes in rainbow trout (Oncorhynchus mykiss).

Although studies have established that exogenous growth hormone (GH) treatment stimulates growth in fish, its effects on target tissue gene expression are not well characterized. We assessed the effects of Posilac (Monsanto, St. Louis, MO), a recombinant bovine GH, on tissue transcript levels in rainbow trout selected from two high-growth rate and two low-growth rate families. Transcript abundance was measured in liver and muscle with the Genome Research in Atlantic Salmon Project (GRASP) 16K cDNA microarray. A selection of the genes identified as altered by the microarray and transcripts for insulin-like growth factors, growth hormone receptors (GHRs), and myostatins were measured by real-time PCR in the liver, muscle, brain, kidney, intestine, stomach, gill, and heart. In general, transcripts identified as differentially regulated in the muscle on the microarray showed similar directional changes of expression in the other nonhepatic tissues. A total of 114 and 66 transcripts were identified by microarray as differentially expressed with GH treatment across growth rate for muscle and liver, respectively. The largest proportion of these transcripts represented novel transcripts, followed by immune and metabolism-related genes. We have identified a number of genes related to lipid metabolism, supporting a modulation in lipid metabolism following GH treatment. Most notable among the growth-axis genes measured by real-time PCR were increases in GHR1 and -2 transcripts in liver and muscle. Our results indicate that short-term GH treatment activates the immune system, shifts the metabolic sectors, and modulates growth-regulating genes.

Endocrine and orexigenic actions of growth hormone secretagogues in rainbow trout (Oncorhynchus mykiss).

The effects of growth hormone secretagogues (GHSs) on the teleost somatotropic axis are poorly understood, particularly with respect to insulin-like growth factor-I (IGF-I) and the IGF-binding proteins (IGFBPs). To assess the endocrine and orexigenic responses of rainbow trout (Oncorhynchus mykiss) to GHS treatment, animals were injected with human GHRH(1-29)-amide, KP-102 or rat ghrelin at 0, 1 or 10 pmol/g body mass. Feed intake was tested at 2 and 5 h post-injection and plasma levels of growth hormone (GH), IGF-I and the IGFBPs were determined at 3, 6 and 12 h post-injection. Feed intake was significantly elevated by all of the GHSs tested at both post-injection time points. All GHSs elevated plasma GH levels in a time-dependent manner. Plasma IGF-I levels were elevated by all GHSs at 3 h post-injection, whereas those animals treated with KP-102 and ghrelin exhibited depressions at 6 h. Four IGFBPs were identified in the plasma by western blotting. Levels of the 20 kDa IGFBP decreased over the sampling time. Levels of the 32 kDa IGFBP were significantly depressed by all GHSs tested. Levels of the 42 kDa IGFBP were significantly elevated by all GHSs tested. Plasma levels of the 50 kDa IGFBP was decreased in some treatment groups at 3 h, but elevated by 6 h in the ghrelin-treated groups and elevated in all treatment groups by 12 h post-injection. The endocrine and orexigenic responses demonstrate that GHSs influence the teleost neuroendocrine system beyond short-term actions (<3 h post-injection) on GH release and the responses of the IGFBPs to GHS treatment support this notion and clarify their identification as functional homologues to mammalian IGFBPs.

Discordant regulation of hepatic IGF-I mRNA and circulating IGF-I during compensatory growth in a teleost, the hybrid striped bass (Morone chrysopsxMorone saxatilis).

Compensatory growth (CG) is a period of growth that exceeds normal rates after animals are alleviated of certain growth-stunting conditions. Little is known, however, about the endocrine control of CG in teleosts. So, our aim was to induce CG in juvenile hybrid striped bass (HSB, Morone chrysopsxMorone saxatilis) through manipulations in feeding regimen, and then determine whether changes in circulating insulin-like growth factor-I (IGF-I) and hepatic IGF-I gene expression accompany the CG response. A considerable catabolic state was induced in HSB fed a total of two times over 4 weeks (once each in the 2nd and 3rd week). Negative energy balance was evidenced through weight loss (-3.4% BW) and a significant drop in hepatosomatic index (HSI) from a value of 3.71 to 1.46. Upon realimentation, in which HSB were fed ad libitum 2x/day, a significant CG response was observed over a 4-week period. The CG response was characterized by an elevated specific growth rate, hyperphagia, restoration of the HSI and an improvement in feed conversion, all relative to controls that were fed ad libitum 2x/day throughout the experiment. Moreover, the CG response and catabolic state preceding it were marked by a discordant regulation in the expression of hepatic IGF-I mRNA and plasma IGF-I levels, the latter parameter paralleling changes in growth (r(2)=0.56, P<001). The catabolic state was accompanied by an 82% increase in hepatic IGF-I mRNA while levels of plasma IGF-I were significantly depressed relative to controls. During the subsequent CG response, however, hepatic IGF-I mRNA decreased by 61% while plasma IGF-I increased by 86%. The underlying mechanisms for this inverse regulation of hepatic IGF-I mRNA and circulating IGF-I are uncertain, but may reflect alterations in hepatic IGF-I mRNA production, stability, and translation such that hepatic IGF-I mRNA is accumulated during periods of catabolism and then rapidly translated and released into circulation when conditions improve. These results suggest that CG can be induced in HSB following a sufficient catabolic state and that systemic IGF-I may be an important mediator of the accelerated growth rate characteristic of CG.