This study was aimed to evaluate the effect of dietary supplementation of lipid-encapsulated (coated) zinc oxide ZnO on post-weaning diarrhea (colibacillosis) in weaned piglets challenged with enterotoxigenic Escherichia coli (ETEC). Thirty-two 35-day-old weaned piglets were orally challenged with 3 × 10(10) colony forming units of ETEC K88 while eight piglets received no challenge (control). Each eight challenged piglets received a diet containing 100 ppm ZnO (low ZnO), 2500 ppm ZnO (high ZnO) or 100 ppm of lipid (10%)-coated ZnO (coated ZnO) for 7 days; control pigs received the low ZnO diet. Daily gain, goblet cell density in the villi of the duodenum, jejunum and ileum, and villus height in the jejunum and ileum, which decreased due to the challenge, were equally greater in the coated ZnO and high ZnO groups versus low ZnO group. Fecal consistency score, serum interleukin-8 concentration, subjective score of fecal E. coli shedding, and digesta pH in the stomach, jejunum and ileum, which increased due to the challenge, were equally low in the coated ZnO and high ZnO groups versus low ZnO. Results suggest that a low level of coated ZnO might well substitute for a pharmacological level of native ZnO in dietary supplementation to alleviate colibacillosis of weaned piglets.

This study compared the effects of varying lipid content and dietary concentration of a lipid-encapsulated (LE) ZnO product to those of native ZnO and thereby to find insights into optimal lipid coating and dosage of the Zn supplement. A total of 192 21-d-old weanling pigs were allotted to 48 pens, after which each six pens received a ZnO-free basal diet supplemented with 125 ppm ZnO (100 ppm Zn; BASAL), 2,500 ppm Zn as native ZnO (HIGH), or 100 or 200 ppm Zn as LE ZnO (LE-100 or LE-250) containing 8%, 10%, or 12% lipid [LE-8%, LE-10%, or LE-12%, respectively; 2 × 3 factorial arrangement within the LE-ZnO diets (LE-ALL)] for 14 d. Forty pigs were killed at the end for histological and biochemical examinations. None of ADG, ADFI, gain:feed, and fecal consistency score differed between the LE-ALL and either of the BASAL and HIGH groups. Hepatic and serum Zn concentrations were greater (p <0.05) in the HIGH vs. LE-ALL group, but did not differ between LE-ALL and BASAL, between LE-100 and -250, or among LE-8%, -10%, and -12% groups. Villus height (VH), crypt depth (CD), and the VH:CD ratio in the duodenum, jejunum, and ileum did not differ between the LE-ALL and either of the BASAL and HIGH groups, except for a greater CD in the duodenum in the LE-ALL vs. HIGH group. Additionally, VH and CD in the duodenum and VH:CD in the jejunum were greater in the LE-250 vs. LE-100 group. Specific activities of sucrase, maltase, and leucine aminopeptidase in these intestinal regions and those of amylase and trypsin in the pancreas were not influenced by the lipid content or dietary concentration of LE ZnO and also did not differ between the LE-ALL and either of the BASAL and HIGH groups, except for a greater pancreatic amylase activity in the former vs. HIGH group. In conclusion, the present results indicate that the LE ZnO, regardless of its lipid percentage or supplementation level examined in this study, has no significant effect on growth performance, fecal consistency, or digestive enzyme activities of weanling pigs under the experimental conditions.

† These authors contributed equally to this work.Abstract. The present study was designed to determine the effects of leptin on lipid metabolism and gene expression during differentiation and maturation of the 3T3-L1 murine preadipocyte. The preadipocytes were induced to differentiate in a growth medium containing 10% calf serum and a hormonal cocktail for 2 days. The cells were next allowed to maturate for 14 days in the growth medium supplemented with 10 μg/ml insulin or 500 ng/ml insulin-like growth factor (IGF)-I in the absence or presence of supplemented leptin. Leptin, at a dose of 5 to 500 ng/ml, had no effect on proliferation of undifferentiated 3T3-L1 cells. However, leptin suppressed the insulin-or IGF-I-stimulated lipid accumulation and enhanced the release of glycerol, a measure of lipolysis, in a dose-dependent manner during and after the maturation of the cell. Moreover, leptin at a dose of 50 ng/ml inhibited IGF-I gene expression during the entire differentiation and maturation and also peroxisome proliferator activated receptor (PPAR)-γ expression during late maturation as monitored by semi-quantitative reverse transcription-polymerase chain reaction. However, leptin exerted no effect on the expression of transforming growth factor-β, CCAT/enhancer binding protein-α and PPAR-δ. Taken together, results suggest the anti-lipogenic and lipolytic effects of leptin in differentiating and mature adipocytes may have been partly mediated by suppressing the expression of PPAR-γ and IGF-I genes.Key words: Leptin, IGF-I, PPAR, Adipocyte, Differentiation, Lipid (Endocrine Journal 55: 827-837, 2008) ADIPOCYTES are highly specialized cells which play an important role in energy homeostasis by harboring energy reservoirs as lipid droplets consisting of triglycerides [1,2]. These reservoirs, however, have been implicated in a host of major human health problems, because an excessive or insufficient energy reserve results in a metabolic disorder known as obesity or lipodystrophy, respectively [3,4]. The cellular development and subsequent metabolic processes controlling the energy reserve of adipocdytes are regulated by a number of transcription factors and autocrine/paracrine as well as endocrine agents. Insulinlike growth factor (IGF)-I stimulates the proliferation and differentiation including lipid synthesis and also inhibits lipolysis in the adipose cell lines in a fashion similar to that of insulin [5][6][7]. Transforming growth factor-β also has a stimulatory effect on proliferation of preadipocytes [8], but, unlike IGF-I, this peptide inhibits differentiation of preadipocyte cell lines [9,

Background and AimAlthough a liver transplantation is considered to be the only effective long-term treatment in many cases of liver diseases, it is limited by a lack of donor organs and immune rejection. As an autologous stem cell approach, this study was conducted to assess whether forkhead box A2 (Foxa2) gene overexpression in bone marrow-derived mesenchymal stem cells (MSC) could protect the liver from hepatic diseases by stimulating tissue regeneration after cell transplantation.MethodsRat MSC (rMSC) were isolated, characterized, and induced to hepatocytes that expressed liver-specific markers. Four different treatments (control [phosphate-buffered saline], rMSC alone, rMSC/pIRES–enhanced green fluorescent protein (EGFP) vector, and rMSC/pIRES–EGFP/human Foxa2) were injected into the spleen of carbon tetrachloride-injured rats. Biochemical and histological analyses on days 30, 60, and 90 post-transplantation were performed to evaluate the therapeutic capacities of MSC overexpressing hFoxa2.ResultsrMSC transfected with hFoxa2 were induced into hepatogenic linage and expressed several liver-specific genes, such as, Foxa2, α-fetoprotein, cytokeratin-18, hepatocyte nuclear factor-1α, and hepatocyte growth factor. A group of animals treated with MSC/hFoxa2 showed significant recovery of liver-specific enzyme expressions to normal levels at the end of the study (90 days). Furthermore, when compared to the fibrotic areas of the samples treated with MSC alone or MSC/vector, the fibrotic area of the samples treated with rMSC/hFoxa2 for 90 days significantly decreased, until they were completely gone.ConclusionsHuman Foxa2 efficiently promoted the incorporation of MSC into liver grafts, suggesting that hFoxa2 genes could be used for the structural or functional recovery of damaged liver cells.

The study was performed to investigate the effect of dietary supplementation of a lipid-encapsulated Zinc oxide on growth parameters and intestinal mucosal morphology piglets born to Duroc-sired Landrace × Yorkshire dams. Twenty-four 30-day-old piglets weaned at 25 days of age were orally challenged with 5 × 108 colony forming units of enterotoxigenic Escherichia coli (ETEC) K88 and fed one of the four diets for 7 days: (i) a nursery basal diet containing 100-ppm ZnO (referred to as BASAL), (ii) BASAL supplemented with 120-ppm apramycin (referred to as ANTIBIO), (iii) BASAL with 2,400-ppm ZnO (referred to as HIGH), and BASAL containing 100-ppm lipid-encapsulated ZnO (referred to as LE). All piglets were killed at the end of the experiment for histological examination on the intestine. The results showed that the average daily gain (ADG), the villus height: crypt depth (CD) ratio in the ileum, and the goblet cell density of the villus and crypt in the duodenum, jejunum, and colon were greater in the LE-fed group that those of the BASAL (p < 0.05). Fecal consistency score (FCS) and the CD ratio in the ileum were less in the LE-fed group, compared to the BASAL-fed one (p < 0.05). The effects observed in the LE-fed group were almost equal to those of the HIGH-fed group as well as even superior to those of the ANTIBIO-fed group. Taken together, our results imply that dietary supplementation of 100-ppm lipid-encapsulated ZnO is as effective as that of 2,400-ppm ZnO for promoting growth diarrhea and intestinal morphology caused by ETEC infection.