There are several constraints to of the sustainability of the livestock industries in different areas of the world. The two most obvious hurdles to high dairy production are diseases during the transition period and heat stress (HS). Despite decades of research, the actual pathologies of ketosis and HS remain poorly understood. In the US, it was estimated that the economic losses from ketosis is $360/cow/cycle, and to HS was ~ $900 million per year. Thus, both severely jeopardize the competitiveness of animal agriculture. Regardless of the herd size, HS and ketosis affect every dairy region in the country. The biological investigations of ketosis and HS have been studied for more than 50 years, but the negative impacts of both are as severe today as they were 30 years ago.

In the current dissertation, ketosis in dairy cows and HS in pigs and steers were investigated to better understand the biology and etiology of both disorders. Study 1 (Chapter 2) was conducted to characterize biomarkers of inflammation during the transition period in healthy and clinically diagnosed ketotic cows. The results indicated that circulating NEFA and BHBA were increased and milk yield was decreased in ketotic relative to healthy cows. In addition, pre-calving circulating LPS was increased twofold in cows that were diagnosed with ketosis post-calving compared to healthy cows, but no LPS differences were detected post-partum. Post-calving LPB, SAA and Hp were increased when compared with their healthy counterparts. Our data suggest the development of ketosis may be intimately linked to inflammation and our selection criteria suggest that intestinal permeability may be the origin of maladaptation to lactation.

In Study 2 (Chapter 3) we investigated the effects of a mineral supplement (zinc amino acid complex) on temporal biomarkers of intestinal integrity and intestinal morphology in heat-stressed steers. As expected, HS increased thermal indices and decreased feed intake. However, steers supplemented with zinc amino acid complex had decreased rectal temperature, improved biomarkers of leaky gut (haptoglobin, and LBP), altered intestinal morphology (decreasing duodenum villi width, increasing jejunum villi height and jejunum and ileum villi height:crypt depth), and improvement in some of the blood gas variables relative to steers supplemented with zinc sulfate. Altogether, the findings of Study 2 demonstrated that a Zn-amino acid complex may mediate some of the negative effects of HS in a growing ruminant model.

Study 3 (Chapter 4) investigated the temporal pattern of metabolic variables and biomarkers associated with intestinal barrier dysfunction during recovery from HS in pigs. Similar to Study 2, HS increased thermal indices and decreased feed intake. Circulating glucose decreased during HS and remained low for 3 d following HS. The insulin:feed intake tended to be increased during HS, and LBP increased linearly during HS recovery. In addition, HS decreased villous height in both jejunum and ileum but intestinal morphology mostly returned to normal following 3 days of recovery. The results of this study confirmed the negative effects of HS on thermal indices, inflammatory biomarkers, and intestinal morphology; however, it suggests that intestinal integrity was restored fairly quickly, but the acute phase protein response increased with time following HS exposure.

In conclusion, the results of the aforementioned studies indicate a negative association of impaired gut integrity with the incidence of ketosis in transitioning dairy cows and performance in heat-stressed steers and pigs. A better understanding of the relative contribution of the intestinal barrier dysfunction to ketosis and heat-induced effects on metabolism and gut morphology is a prerequisite for designing targeted strategies to alleviate the negative consequences of ketosis and HS on farm animals’ productivity.