Excessive rates of demand lipolysis in the adipose tissue (AT) during periods of negative energy balance (NEB) are associated with increased susceptibility to disease and limited lactation performance. Lipolysis induces a remodeling process within AT that is characterized by an inflammatory response, cellular proliferation, and changes in the extracellular matrix (ECMT). The adipose tissue macrophage (ATM) is a key component of the inflammatory response. Infiltration of ATM-forming cellular aggregates was demonstrated in transition cows, suggesting that ATM trafficking and phenotype changes may be associated with disease. However, it is currently unknown if ATM infiltration occurs in dairy cows only during NEB states related to the transition period or also during NEB-induced lipolysis at other stages of lactation. The objective of this study was to evaluate changes in ATM trafficking and inflammatory phenotypes, and the expression of genetic markers of AT remodeling in healthy late-lactation cows during feed restriction-induced NEB. After a 14-d (d −14 to d −1) preliminary period, Holstein cows were randomly assigned to 1 of 2 feeding protocols, ad libitum (AL) or feed restriction (FR), for 4 d (d 1-4). Caloric intake was reduced in FR to achieve a targeted energy balance of −15 Mcal/d of net energy for lactation. Omental and subcutaneous AT samples were collected laparoscopically to harvest stromal vascular fraction (SVF) cells on d −3 and 4. The FR induced a NEB of −14.1 ± 0.62 Mcal/d of net energy for lactation, whereas AL cows remained in positive energy balance (3.2 ± 0.66 Mcal/d of NE L ). The FR triggered a lipolytic response reflected in increased plasma nonesterified fatty acids (0.65 ± 0.05 mEq/L on d 4), enhanced phosphorylation of hormone sensitive lipase, and reduced adipocyte diameter.Flow cytometry and immunohistochemistry analysis revealed that on d 4, FR cows had increased numbers of CD172a + , an ATM (M1 and M2) surface marker, cells in SVF that were localized in aggregates. However, FR did not alter the number of SVF cells expressing M1 markers (CD14 and CD11c) or M2 markers (CD11b and CD163). This finding contrasts with the predominately M1 phenotype observed previously in ATM from clinically diseased cows. No changes were observed in the expression of ECMT-related or cell proliferation markers. In summary, an acute 4-d lipolytic stimulus in late-lactation dairy cows led to ATM infiltration with minimal changes in inflammatory phenotype and no changes in ECMT. These results underscore that physiological changes related to parturition, the onset of lactation, extended periods of lipolysis, or a combination of these can induce intense AT remodeling with enhanced ATM inflammatory phenotype expression that may impair the metabolic function of AT in transition dairy cattle.

Mast cell (MC)-associated diseases, including allergy/anaphylaxis and neuroinflammatory pain disorders, exhibit a sex bias, with females at increase risk. While much attention has been directed toward adult sex hormones as drivers of sex differences, that female sex bias in MC-associated diseases is evident in prepubertal children, suggesting early-life origins of sex differences which have yet to be explored. Utilizing rodent models of MC-mediated anaphylaxis, our data here reveal that, 1) compared with females, males exhibit significantly reduced severity of MC-mediated anaphylactic responses that emerge prior to puberty and persist into adulthood, 2) reduced severity of MC-mediated anaphylaxis in males is linked with the naturally high level of perinatal androgens and can be recapitulated in females by perinatal exposure to testosterone proprionate, 3) perinatal androgen exposure guides bone marrow MC progenitors toward a masculinized tissue MC phenotype characterized by decreased concentration of prestored MC granule mediators (e.g., histamine, serotonin, and proteases) and reduced mediator release upon degranulation, and 4) engraftment of MC-deficient KitW-sh/W-sh mice with adult male, female, or perinatally androgenized female MCs results in MC-mediated anaphylaxis response that reflects the MC sex and not host sex. Together, these data present evidence that sex differences in MC phenotype and resulting disease severity are established in early life by perinatal androgens. Thus, factors affecting levels of perinatal androgens could have a significant impact on MC development and MC-associated disease risk across the life span.

There are sex associated differences in the risk for cardiovascular comorbidities in obesity and metabolic syndrome. A common clinical finding in these diseases is the expansion of perivascular adipose tissues (PVAT) which is associated with alterations in their role as regulators of vessel function. PVAT hyperplasia and hypertrophy are dependent on the biology of populations of adipocyte progenitor cells (APC). It is currently unclear if PVAT enlargement diverges between males and females and the mechanisms linking APC biology with sexual dimorphism remain poorly understood. This study tested the hypothesis that vessel location and sexual dimorphism affect the distribution and adipogenic capacity of APC in cardiovascular disease risk relevant PVAT sites. PVAT from thoracic aorta (aPVAT) and mesenteric resistance arteries (mPVAT) was collected from 10‐week‐old female and male Sprague–Dawley rats. Differences in APC distribution in stromal vascular fraction cells from PVAT were determined. APC were defined as cells expressing CD34, CD44, and platelet derived growth factor α. In both sexes aPVAT had fewer APC compared to mPVAT and perigonadal adipose tissue (GON). Sex‐related differences were observed in the expression of CD34, where females had fewer CD34+ cells in PVATs. APC proliferation and adipogenic capacity in vitro were not affected by sex. However, APC from aPVAT had a lower proliferation capacity compared to mPVAT. These data demonstrate that the distribution of APC within PVAT exhibits sexual dimorphism and is affected by anatomical location.

A study was conducted to evaluate the effects of a multi-strain Bacillus subtilis-based direct-fed microbial (DFM) on growth performance and apparent nutrient digestibility of nursery pigs. Eighty pigs, of equal number of barrows and gilts (initial BW: 7.0 ± 0.60 kg), were weaned at 21 ± 1 d and randomly allotted to one of sixteen pens, with five pigs per pen. Two dietary treatments were implemented, a basal control (CON) and a control plus DFM (DFM). Both diets were corn, soybean meal, and distillers dried grains based. Diets were fed for 42 d and growth performance measures were recorded weekly. On d 21 and 42 of the experiment, one pig per pen, with equal number of males and females, was randomly selected and euthanized. Digestibility of nitrogen (N), amino acids (AA) and energy were evaluated within the duodenum, jejunum, ileum, ascending and distal colon. Relative to CON, DFM tended to increase ADG during wk 2 (P = 0.08), and significantly increased ADFI during wk 2 (P = 0.04) and wk 3 (P = 0.02). In addition, DFM decreased G:F during wk 6, relative to CON (P = 0.04). Within the jejunum, pigs fed DFM had greater digestibility of tryptophan (P = 0.04) and cysteine (P = 0.04), and tended to have greater digestibility of lysine (P = 0.07), methionine (P = 0.06), and threonine (P = 0.08), relative to CON. The content pH in ascending colon did not differ between DFM and CON. Compared to CON, apparent total tract digestibility (ATTD) of energy of DFM did not differ while ATTD of nitrogen of DFM was lower (P = 0.05). The addition of a multi-strain Bacillus subtilis-based DFM appears to impact growth performance, AA and N digestibility depending upon location in the gastrointestinal tract, with primary AA differences occurring within the mid-jejunum.

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