Omega-3 fatty acids have immunomodulatory and anti-inflammatory effects. The objective of this project was to determine the effects of fish oil, a source of omega-3 fatty acids, on genes involved in inflammation and growth of skeletal muscle tissue after an LPS challenge. Male Landrace-New Hampshire weaned piglets (BW 8.21±0.83 kg) were used in a randomized complete block design and assigned to two treatments: 1) basal diet (n=7) and 2) basal diet plus 3% fish oil added (n = 7). Treatments were fed for 35 d. On d 34, an LPS challenge was performed and 24 h later, piglets were euthanized and skeletal muscle samples were collected from the longissimus lumborum and biceps femoris. Total mRNA was isolated and markers of inflammation [cyclophilin (Cyclo), nuclear factor kappa beta subunit-1 (NF-kB), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)], skeletal muscle growth [paired box transcription factor-7 (Pax7), myogenic factor-5 (Myf5), myoblast determination factor-1 (MyoD), myogenin (MyoG)] and adipose growth (peroxisome proliferator activated receptor (PPARy), leptin, and adiponectin) were analyzed. Cyclophilin abundance was increased (P = 0.03) in fish-oil piglets compared to control piglets. Other markers of inflammation (TNF-α, IL-6, NF-kB) were not affected (P > 0.05) by fish-oil supplementation. Abundance of Myf5 was lower (P = 0.03) in fish oil piglets than control piglets. Other myogenic regulatory factors (Pax7, MyoD, MyoG) were not (P > 0.05) altered by treatment. Abundance of PPARy, leptin or adiponectin was not affected (P > 0.05) by fish-oil supplementation. Muscle location influenced (P < 0.01) abundance of leptin and adiponectin, with abundance being higher in the biceps femoris than in the longissimus lumborum. No other genes analyzed were impacted by muscle location (P > 0.05). Our findings suggest that supplementation of omega-3 fatty acids via fish-oil may affect the inflammatory response and skeletal muscle growth. Further research is needed to evaluate the impact of these results on animal production.
Advanced paternal age has increasingly been recognized as a risk factor for male fertility and progeny health. While underlying causes are not well understood, aging is associated with a continuous decline of blood and tissue NAD+ levels, as well as a decline of testicular functions. The important basic question to what extent ageing-related NAD+ decline is functionally linked to decreased male fertility has been difficult to address due to the pleiotropic effects of aging, and the lack of a suitable animal model in which NAD+ levels can be lowered experimentally in chronologically young adult males. We therefore developed a transgenic mouse model of acquired niacin dependency (ANDY), in which NAD+ levels can be experimentally lowered using a niacin-deficient, chemically defined diet. Using ANDY mice, this report demonstrates for the first time that decreasing body-wide NAD+ levels in young adult mice, including in the testes, to levels that match or exceed the natural NAD+ decline observed in old mice, results in the disruption of spermatogenesis with small testis sizes and reduced sperm counts. ANDY mice are dependent on dietary vitamin B3 (niacin) for NAD+ synthesis, similar to humans. NAD+-deficiency the animals develop on a niacin-free diet is reversed by niacin supplementation. Providing niacin to NAD+-depleted ANDY mice fully rescued spermatogenesis and restored normal testis weight in the animals. The results suggest that NAD+ is important for proper spermatogenesis and that its declining levels during aging are functionally linked to declining spermatogenesis and male fertility. Functions of NAD+ in retinoic acid synthesis, which is an essential testicular signaling pathway regulating spermatogonial proliferation and differentiation, may offer a plausible mechanism for the hypospermatogenesis observed in NAD+-deficient mice.
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