Heat stress negatively influences the global pork industry and undermines genetic, nutritional, management and pharmaceutical advances in management, feed and reproductive efficiency. Specifically, heat stress-induced economic losses result from poor sow performance, reduced and inconsistent growth, decreased carcass quality, mortality, morbidity, and processing issues caused by less rigid adipose tissue (also known as flimsy fat). When environmental conditions exceed the pig’s thermal neutral zone, nutrients are diverted from product synthesis (meat, fetus, milk) to body temperature maintenance thereby compromising efficiency. Unfortunately, genetic selection for both increased litter size and leaner phenotypes decreases pigs’ tolerance to heat, as enhanced fetal development and protein accretion results in increased basal heat production. Additionally, research has demonstrated that in utero heat stress negatively and permanently alters post-natal body temperature and body composition and both variables represent an underappreciated consequence of heat stress. Advances in management (i.e. cooling systems) have partially alleviated the negative impacts of heat stress, but productivity continues to decline during the warm summer months. The detrimental effects of heat stress on animal welfare and production will likely become more of an issue in regions most affected by continued predictions for climate change, with some models forecasting extreme summer conditions in key animal-producing areas of the globe. Therefore, heat stress is likely one of the primary factors limiting profitable animal protein production and will certainly continue to compromise food security (especially in emerging countries) and regionalise pork production in developed countries. Thus, there is an urgent need to have a better understanding of how heat stress reduces animal productivity. Defining the biology of how heat stress jeopardises animal performance is critical in developing approaches (genetic, managerial, nutritional and pharmaceutical) to ameliorate current production issues and improve animal wellbeing and performance.

Although pigs are used widely as models of human disease, their utility as models has been enhanced by genetic engineering. Initially, transgenes were added randomly to the genome, but with the application of homologous recombination, zinc finger nucleases, and transcription activator-like effector nuclease (TALEN) technologies, now most any genetic change that can be envisioned can be completed. To date these genetic modifications have resulted in animals that have the potential to provide new insights into human diseases for which a good animal model did not exist previously. These new animal models should provide the preclinical data for treatments that are developed for diseases such as Alzheimer’s disease, cystic fibrosis, retinitis pigmentosa, spinal muscular atrophy, diabetes, and organ failure. These new models will help to uncover aspects and treatments of these diseases that were otherwise unattainable. The focus of this review is to describe genetically engineered pigs that have resulted in models of human diseases.

Manganese (Mn) is the twelfth most abundant element in the earth's crust and is widely distributed throughout the surface of the planet, naturally occurring in rocks, soil, water, and food. As an essential trace mineral in diets, Mn is required for a variety of metabolic functions including skeletal system development, energy metabolism, enzyme activation, nervous system function, immune system function, and reproductive hormone function. Manganese has effects on reproductive hormone function as a cofactor for enzymes necessary for cholesterol synthesis. Production of steroid hormones necessary for reproduction is dependent on the availability of cholesterol as a precursor. There is also evidence that Mn has effects on reproduction due to actions at the hypothalamus. Because Mn is used for manufacturing of steel, recent research has focused on the effects of Mn toxicity as a result of occupational endeavors rather than evaluating the optimal Mn inclusion rate for mammalian growth and development, reproductive function, immune function, etc. The objective of this review is to address the functions of Mn in reproduction of animals but there is also a focus on other areas of mammalian biology affected by Mn functions, with an emphasis on domestic swine (Sus scrofa).

Hyperthermia or heat stress (HS) occurs when heat dissipation mechanisms are overwhelmed by external and internal heat production. Hyperthermia negatively affects reproduction and potentially compromises oocyte integrity and reduces developmental competence of ensuing embryos. Autophagy is the process by which cells recycle energy through the reutilization of cellular components and is activated by a variety of stressors. Study objectives were to characterize autophagy-related proteins in the ovary following cyclical HS during the follicular phase. Twelve gilts were synchronized and subjected to cyclical HS (n = 6) or thermal neutral (n = 6) conditions for 5 days during the follicular phase. Ovarian protein abundance of Beclin 1 and microtubule associated protein light chain 3 beta II were each elevated as a result of HS (P = 0.001 and 0.003, respectively). The abundance of the autophagy related (ATG)12–ATG5 complex was decreased as a result of HS (P = 0.002). Regulation of autophagy and apoptosis occurs in tight coordination, and B-cell lymphoma (BCL)2 and BCL2L1 are involved in regulating both processes. BCL2L1 protein abundance, as detected via immunofluorescence, was increased in both the oocyte (∼1.6-fold; P < 0.01) and granulosa cells of primary follicles (∼1.4-fold P < 0.05) of HS ovaries. These results suggest that ovarian autophagy induction occurs in response to HS during the follicular phase, and that HS increases anti-apoptotic signaling in oocytes and early follicles. These data contribute to the biological understanding of how HS acts as an environmental stress to affect follicular development and negatively impact reproduction.

The study objectives were to test the hypothesis that heat stress (HS) during gestational development alters postnatal growth, body composition, and biological response to HS conditions in pigs. To investigate this, 14 first parity crossbred gilts were exposed to one of four environmental treatments (TNTN, TNHS, HSTN, or HSHS) during gestation. TNTN and HSHS dams were exposed to thermal neutral (TN, cyclical 18–22°C) or HS conditions (cyclical 28–34°C) during the entire gestation, respectively. Dams assigned to HSTN and TNHS treatments were heat-stressed for the first or second half of gestation, respectively. Postnatal offspring were exposed to one of two thermal environments for an acute (24 h) or chronic (five weeks) duration in either constant TN (21°C) or HS (35°C) environment. Exposure to chronic HS during their growth phase resulted in decreased longissimus dorsi cross-sectional area (LDA) in offspring from HSHS and HSTN treated dams whereas LDA was larger in offspring from dams in TNTN and TNHS conditions. Irrespective of HS during prepubertal postnatal growth, pigs from dams that experienced HS during the first half of gestation (HSHS and HSTN) had increased (13.9%) subcutaneous fat thickness compared to pigs from dams exposed to TN conditions during the first half of gestation. This metabolic repartitioning towards increased fat deposition in pigs from dams heat-stressed during the first half of gestation was accompanied by elevated blood insulin concentrations (33%; P = 0.01). Together, these results demonstrate HS during the first half of gestation altered metabolic and body composition parameters during future development and in biological responses to a subsequent HS challenge.