A survey of parasites in freshwater fishes from Nong Han wetland, Udon Thani Province, Thailand.

The diversity of fish parasites from freshwater fishes collected from the Nong Han wetland (Udon Thani Province, Thailand) was studied by visually examining 22 freshwater fish species (253 samples) from 19 genera for external and internal parasites. A majority of fishes in the Nong Han wetland were infected by parasites (75.89%). Twenty fish species (75.89%) were infected with a total of 29 species of parasites. These included 9 species of monogeneans, 5 crustaceans, 5 acanthocephalans, 4 nematodes, 3 digeneans, and 3 species of cestodes. Cyclocheilichthys apogon had the most diverse parasite community (8 species). Seasons affected the prevalence and mean intensity of parasitic infection; the prevalence was highest during the rainy (85.54%) and winter (84.75%) seasons, and lower during the summer (63.96%) season. Fish diversity and parasite diversity exhibited a positive correlation relationship. In the light of declining fish populations in the Nong Han wetland, this study may provide critical information for the sustainable management of this wetland. Furthermore, some of the identified fish parasites can be harmful to humans if fish is eaten raw or improperly cooked, as is the tradition in northeastern Thailand, so our findings may bear relevance for public health workers as well.

Gene expression patterns indicate that a high-fat-high-carbohydrate diet causes mitochondrial dysfunction in fish.

Expensive and unsustainable fishmeal is increasingly being replaced with cheaper lipids and carbohydrates as sources of energy in aquaculture. Although it is known that the excess of lipids and carbohydrates has negative effects on nutrient utilization, growth, metabolic homeostasis, and health of fish, our current understanding of mechanisms behind these effects is limited. To improve the understanding of diet-induced metabolic disorders (both in fish and other vertebrates), we conducted an eight-week high-fat-high-carbohydrate diet feeding trial on blunt snout bream (Megalobrama amblycephala), and studied gene expression changes (transcriptome and qPCR) in the liver. Disproportionately large numbers of differentially expressed genes were associated with mitochondrial metabolism, neurodegenerative diseases (Alzheimer's, Huntington's, and Parkinson's), and functional categories indicative of liver dysfunction. A high-fat-high-carbohydrate diet may have caused mitochondrial dysfunction, and possibly downregulated the mitochondrial biogenesis in the liver. While the relationship between diet and neurodegenerative disorders is well-established in mammals, this is the first report of this connection in fish. We propose that fishes should be further explored as a potentially promising model to study the mechanisms of diet-associated neurodegenerative disorders in humans.

Metabolite and gene expression profiles suggest a putative mechanism through which high dietary carbohydrates reduce the content of hepatic betaine in Megalobrama amblycephala.

BACKGROUND: High-carbohydrate diets (HCD) are favoured by the aquaculture industry for economic reasons, but they can produce negative impacts on growth and induce hepatic steatosis. We hypothesised that the mechanism behind this is the reduction of hepatic betaine content. OBJECTIVE: We further explored this mechanism by supplementing betaine (1%) to the diet of a farmed fish Megalobrama amblycephala. METHODS: Four diet groups were designed: control (CD, 27.11% carbohydrates), high-carbohydrate (HCD, 36.75% carbohydrates), long-term betaine (LBD, 35.64% carbohydrates) and short-term betaine diet (SBD; 12 weeks HCD + 4 weeks LBD). We analysed growth performance, body composition, liver condition, and expression of genes and profiles of metabolites associated with betaine metabolism. RESULTS: HCD resulted in poorer growth and liver health (compared to CD), whereas LBD improved these parameters (compared to HCD). HCD induced the expression of genes associated with glucose, serine and cystathionine metabolisms, and (non-significantly, p = .20) a betaine-catabolizing enzyme betaine-homocysteine-methyltransferase; and decreased the content of betaine, methionine, S-adenosylhomocysteine and carnitine. Betaine supplementation (LBD) reversed these patterns, and elevated betaine-homocysteine-methyltransferase, S-adenosylmethionine and S-adenosylhomocysteine (all p ≤ .05). CONCLUSION: We hypothesise that HCD reduced the content of hepatic betaine by enhancing the activity of metabolic pathways from glucose to homocysteine, reflected in increased glycolysis, serine metabolism, cystathionine metabolism and homocysteine remethylation. Long-term dietary betaine supplementation improved the negative impacts of HCD, inculding growth parameters, body composition, liver condition, and betaine metabolism. However, betaine supplementation may have caused a temporary disruption in the metabolic homeostasis.

Transcriptomics, metabolomics and histology indicate that high-carbohydrate diet negatively affects the liver health of blunt snout bream (Megalobrama amblycephala).

BACKGROUND: Global trend of the introduction of high levels of relatively cheap carbohydrates to reduce the amount of costly protein in the aquatic animal feed production has affected the aquaculture of an economically important cyprinid fish, blunt snout bream (Megalobrama amblycephala). This dietary shift has resulted in increased prevalence of metabolic disorders, often causing economic losses. High dietary intake of carbohydrates, associated with obesity, is one of the major causes of non-alcoholic fatty liver disease (NAFLD) in humans. RESULTS: We have conducted an eight-week feeding trial to better understand how a high-carbohydrate diet (HCBD) affects the liver health in this fish. Hepatosomatic index and lipid content were significantly (P < 0.05) higher in the HCBD group. Histology results also suggested pathological changes in the livers of HCBD group, with excessive lipid accumulation and indication of liver damage. Metabolomics and serum biochemistry analyses showed that a number of metabolites indicative of liver damage were increased in the HCBD group. This group also exhibited low levels of betaine, which is a metabolite crucial for maintaining the healthy liver functions. Transcriptomic and qPCR analyses indicated that HCBD had a strong impact on the expression of a large number of genes associated with the NAFLD and insulin signalling pathways, which may lead to the development of insulin resistance in hepatocytes, pathological liver changes, and eventually the NAFLD. CONCLUSIONS: Transcriptomics, metabolomics and histology results all indicate early symptoms of liver damage. However whether these would actually lead to the development of NAFLD after a longer period of time, remains inconclusive. Additionally, a very high number of upregulated genes in the HCBD group associated with several neurodegenerative diseases is a strong indication of neurodegenerative changes caused by the high-carbohydrate diet in blunt snout bream. This suggests that fish might present a good model to study neurodegenerative changes associated with high-carbohydrate diet in humans.