Effects of heat stress and insulin sensitizers on pig adipose tissue.

Heat stress (HS) negatively impacts several swine production variables, including carcass fat quality and quantity. Pigs reared in HS have more adipose tissue than energetically predicted, explainable, in part, by HS-induced hyperinsulinemia. Study objectives were to evaluate insulin's role in altering fat characteristics during HS via feeding insulin-sensitizing compounds. Forty crossbred barrows (113 ± 9 kg BW) were randomly assigned to one of five environment by diet treatments: 1) thermoneutral (TN) fed ad libitum (TNAL), 2) TN and pair-fed (TNPF), 3) HS fed ad libitum (HSAL), 4) HS fed ad libitum with sterculic oil (SO) supplementation (HSSO; 13 g/d), and 5) HS fed ad libitum with dietary chromium (Cr) supplementation (HSCr; 0.5 mg/d; Kemin Industries, Des Moines, IA). The study consisted of three experimental periods (P). During P0 (2 d), all pigs were exposed to TN conditions (23 ± 3 °C, 68 ± 10% RH) and fed ad libitum. During P1 (7 d), all pigs received their respective dietary supplements, were maintained in TN conditions, and fed ad libitum. During P2 (21 d), HSAL, HSSO, and HSCr pigs were fed ad libitum and exposed to cyclical HS conditions (28 to 33 °C, 58 ± 10% RH). The TNAL and TNPF pigs remained in TN conditions and were fed ad libitum or pair-fed to their HSAL counterparts. Rectal temperature (TR), respiration rate (RR), and skin temperature (TS) were obtained daily at 0600 and 1800 h. At 1800 h, HS exposed pigs had increased TR, RR, and TS relative to TNAL controls (1.13 °C, 48 bpm, and 3.51 °C, respectively; P < 0.01). During wk 2 and 3 of P2, HSSO pigs had increased 1800 h TR relative to HSAL and HSCr (~0.40 and ~0.42 °C, respectively; P ≤ 0.05). Heat stress decreased ADFI and ADG compared to TNAL pigs (2.24 vs. 3.28 and 0.63 vs. 1.09 kg/d, respectively; P < 0.01) and neither variable was affected by SO or Cr supplementation. Heat stress increased or tended to increase moisture content of abdominal (7.7 vs. 5.9%; P = 0.07) and inner s.c. (11.4 vs. 9.8%; P < 0.05) adipose depots compared to TNAL controls. Interestingly, TNPF pigs also had increased adipose tissue moisture content and this was most pronounced in the outer s.c. depot (15.0 vs. 12.2%; P < 0.01) compared to TNAL pigs. Heat stress had little or no effect on fatty acid composition of abdominal, inner, and outer s.c. adipose tissue depots. In summary, the negative effects of HS on fat quality do not appear to be fatty acid composition related, but may be explained by increased adipose tissue moisture content.

A dose-response evaluation of rumen-protected niacin in thermoneutral or heat-stressed lactating Holstein cows.

Twenty-four multiparous high-producing dairy cows (40.0±1.4kg/d) were used in a factorial design to evaluate effects of 2 environments [thermoneutral (TN) and heat stress (HS)] and a dose range of dietary rumen-protected niacin (RPN; 0, 4, 8, or 12g/d) on body temperature, sweating rate, feed intake, water intake, production parameters, and blood niacin concentrations. Temperature-humidity index values during TN never exceeded 68 (stress threshold), whereas temperature-humidity index values during HS were above 68 for 24h/d. The HS environment increased hair coat and skin, rectal, and vaginal temperatures; respiration rate; skin and hair coat evaporative heat loss; and water intake and decreased DMI (3.5kg/d), milk yield (4.1kg/d), 4% fat-corrected milk (2.7kg/d), and milk protein yield (181.7g/d). Sweating rate increased during HS (12.7g/m(2) per h) compared with TN, but this increase was only 10% of that reported in summer-acclimated cattle. Niacin supplementation did not affect sweating rate, dry-matter intake, or milk yield in either environment. Rumen-protected niacin increased plasma and milk niacin concentrations in a linear manner. Heat stress reduced niacin concentration in whole blood (7.86 vs. 6.89µg/mL) but not in milk. Reduced blood niacin concentration was partially corrected by dietary RPN. An interaction existed between dietary RPN and environment; dietary RPN linearly increased water intake in both environments, but the increase was greater during HS conditions. Increasing dietary RPN did not influence skin temperatures. During TN, supplementing 12g/d of RPN increased hair coat (unshaved skin; 30.3 vs. 31.3°C at 1600h) but not shaved skin (32.8 vs. 32.9°C at 1600h) temperature when compared with 0g/d at all time points, whereas the maximum temperature (18°C) of the room was lower than skin temperature. These data suggest that dietary RPN increased water intake during both TN and HS and hair coat temperature during TN; however, core body temperature was unaffected. Thus, encapsulated niacin did not improve thermotolerance of winter-acclimated lactating dairy cows exposed to moderate thermal stress in Arizona.

Effects of supplemental zinc amino acid complex on gut integrity in heat-stressed growing pigs.

Heat stress (HS) jeopardizes livestock health and productivity and both may in part be mediated by reduced intestinal integrity. Dietary zinc improves a variety of bowel diseases, which are characterized by increased intestinal permeability. Study objectives were to evaluate the effects of supplemental zinc amino acid complex (ZnAA) on intestinal integrity in heat-stressed growing pigs. Crossbred gilts (43±6 kg BW) were ad libitum fed one of three diets: (1) control (ZnC; 120 ppm Zn as ZnSO4; n=13), (2) control+100 ppm Zn as ZnAA (Zn220; containing a total of 220 ppm Zn; n=14), and (3) control+200 ppm Zn as ZnAA (Zn320; containing a total of 320 ppm Zn; n=16). After 25 days on their respective diets, all pigs were exposed to constant HS conditions (36°C, ∼50% humidity) for either 1 or 7 days. At the end of the environmental exposure, pigs were euthanized and blood and intestinal tissues were harvested immediately after sacrifice. As expected, HS increased rectal temperature (P⩽0.01; 40.23°C v. 38.93°C) and respiratory rate (P⩽0.01; 113 v. 36 bpm). Pigs receiving ZnAA tended to have increased rectal temperature (P=0.07; +0.27°C) compared with ZnC-fed pigs. HS markedly reduced feed intake (FI; P⩽0.01; 59%) and caused BW loss (2.10 kg), but neither variable was affected by dietary treatment. Fresh intestinal segments were assessed ex vivo for intestinal integrity. As HS progressed from days 1 to 7, both ileal and colonic transepithelial electrical resistance (TER) decreased (P⩽0.05; 34% and 22%, respectively). This was mirrored by an increase in ileal and colonic permeability to the macromolecule dextran (P⩽0.01; 13- and 56-fold, respectively), and increased colonic lipopolysaccharide permeability (P⩽0.05; threefold) with time. There was a quadratic response (P⩽0.05) to increasing ZnAA on ileal TER, as it was improved (P⩽0.05; 56%) in Zn220-fed pigs compared with ZnC. This study demonstrates that HS progressively compromises the intestinal barrier and supplementing ZnAA at the appropriate dose can improve aspects of small intestinal integrity during severe HS.

Postabsorptive carbohydrate adaptations to heat stress and monensin supplementation in lactating Holstein cows.

Multiparous cows (n=34, 89 d in milk, 537 kg) housed in environmental chambers were fed a control total mixed ration or one containing monensin (450 mg/cow per day) during 2 experimental periods (P): (1) thermal neutral (TN) conditions (constant 20°C) with ad libitum intake for 9 d, and (2) heat stress (HS, n=16) or pair-fed [PF; in TN (PFTN); n=18] for 9 d. Heat-stress was cyclical with temperatures ranging from 29.4 to 38.9°C. Rectal temperatures and respiration rates increased in HS compared with PFTN cows (38.4 to 40.4°C, 40 to 93 breaths/min). Heat stress reduced dry matter intake (DMI, 28%), and by design, PFTN cows had similar intakes. Monensin-fed cows consumed less DMI (1.59 kg/d) independent of environment. Milk yield decreased 29% (9.1 kg) in HS and 15% (4.5 kg) in PFTN cows, indicating that reduced DMI accounted for only 50% of the decreased milk yield during HS. Monensin had no effect on milk yield in either environment. Both HS and PFTN cows entered into calculated negative energy balance (-2.7 Mcal/d), and feeding monensin increased feed efficiency (7%) regardless of environment. The glucose response to an epinephrine (EPI) challenge increased (27%) during P2 for both HS and PFTN cows, whereas the nonesterified fatty acid response to the EPI challenge was larger (56%) during P2 in the PFTN compared with the HS cows. Compared with P1, whole-body glucose rate of appearance (Ra) decreased similarly during P2 in both HS and PFTN cows (646 vs. 514 mmol/h). Although having similar rates of glucose Ra, HS cows synthesized approximately 225 g less milk lactose; therefore, on a milk yield basis, glucose Ra decreased (3.3%) in PFTN but increased (5.6%) in HS cows. Regardless of environment, monensin-fed cows had increased (10%) glucose Ra per unit of DMI. From the results we suggest that the liver remains sensitive but adipose tissue becomes refractory to catabolic signals and that glucose Ra (presumably of hepatic origin) is preferentially utilized for processes other than milk synthesis during HS.

Effects of a supplemental yeast culture on heat-stressed lactating Holstein cows.

Multiparous, lactating Holstein cows (n = 23; 120 +/- 30 d in milk, 690 +/- 67 kg of body weight) housed in climatic chambers were randomly assigned to 1 of 2 dietary treatments: a diet containing a novel yeast culture formulation (YC) for heat stress (n = 12, 10 g/d) or a control diet (n = 11). The trial length was 28 d and consisted of a 7-d thermal neutral period (TN; 18 degrees C, 20% humidity) followed by 21 d of heat stress (HS; cyclical daily temperatures ranging from 29.4 to 37.8 degrees C and 20% humidity). Cows were individually fed a total mixed ration consisting primarily of alfalfa hay and steam-flaked corn. During TN, the YC feeding had no effect on production variables or most body temperature indices. During HS, all body temperature indices increased and YC had no effect on rump surface temperature, respiration rate, or sweating rates. Cows fed YC had lower rectal temperatures at 1200 and 1800 h (40.29 vs. 40.02 degrees C and 40.35 vs. 40.12 +/- 0.07 degrees C, respectively) compared with control-fed cows. Cows fed both diets lost body weight (42 kg) during HS, but there were no differences between diets. Control-fed cows had increased dry matter intake (DMI) and milk yield (19.1 vs. 17.9 +/- 0.5 kg/d and 32.15 vs. 29.15 +/- 0.02 kg/d, respectively) compared with YC-fed cows, but intake and milk production were similar between diets when evaluated on a body weight basis. Heat stress progressively decreased DMI (29%) and milk yield, with milk production reaching a nadir (33%) in the third week. Heat stress decreased milk protein (7%) and lactose (5%) levels, but did not alter milk fat content. Heat-stressed cows were in calculated negative energy balance (-1.91 +/- 0.70 Mcal/d) and this was unaffected by diet. Independent of diet, HS decreased plasma glucose (11%), but neither diet nor HS altered basal nonesterified fatty acid levels. Heat stress increased plasma urea N concentrations (11.5 vs. 14.8 +/- 0.4 mg/dL). Despite YC-fed cows having slightly reduced body temperatures indices, feeding YC did not prevent the negative effects of HS.

Nutritional and developmental regulation of plasma leptin in dairy cattle.

Leptin is thought to play a critical role in regulating energy metabolism throughout mammalian life. In growing dairy cattle, plasma leptin has been proposed as a partial mediator of the effects of nutrition on reproductive and mammary development. However, the developmental stage at which the plane of nutrition increases plasma leptin has not been well defined. Further, it is unknown whether the onset of puberty is affected by plasma leptin concentration in dairy cattle. To investigate these questions, two studies were performed. In the first study, neonatal calves were fed a milk replacer at levels supporting an average daily gain of 570 g/d (L) or 1210 g/d (H). Weekly blood samples were obtained until slaughter at 105 kg of body weight. Plasma leptin and adiposity remained constant in the L calves, but started to increase by the third week of age in the H calves. In the second study, 3- to 5-mo-old heifers were fed a total mixed ration supplemented with either calcium salts of palm fat or conjugated linoleic acids at levels sustaining an average daily gain of approximately 1.0 kg/d. Blood samples were obtained until the third postpubertal luteal phase. The fat source had no effects on growth parameters, body composition, age at puberty, or plasma leptin. Therefore, plasma leptin was reanalyzed as a function of age from start of treatment until slaughter. The plasma concentration of leptin remained nearly constant at 2.3 ng/ml until 1 yr of age, when a rise in plasma leptin became obvious. Puberty occurred with equal frequency either around 1 yr of age when plasma leptin was nearly constant or later when leptin was rising rapidly. We conclude that plasma leptin is regulated by nutrition in early postnatal life, but that a sudden increase in plasma leptin is not required for the onset of puberty in dairy cattle.