Ketogenic diet with medium-chain triglycerides restores skeletal muscle function and pathology in a rat model of Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is an intractable genetic disease associated with progressive skeletal muscle weakness and degeneration. Recently, it was reported that intraperitoneal injections of ketone bodies partially ameliorated muscular dystrophy by increasing satellite cell (SC) proliferation. Here, we evaluated whether a ketogenic diet (KD) with medium-chain triglycerides (MCT-KD) could alter genetically mutated DMD in model rats. We found that the MCT-KD significantly increased muscle strength and fiber diameter in these rats. The MCT-KD significantly suppressed the key features of DMD, namely, muscle necrosis, inflammation, and subsequent fibrosis. Immunocytochemical analysis revealed that the MCT-KD promoted the proliferation of muscle SCs, suggesting enhanced muscle regeneration. The muscle strength of DMD model rats fed with MCT-KD was significantly improved even at the age of 9 months. Our findings suggested that the MCT-KD ameliorates muscular dystrophy by inhibiting myonecrosis and promoting the proliferation of muscle SCs. As far as we can ascertain, this is the first study to apply a functional diet as therapy for DMD in experimental animals. Further studies are needed to elucidate the underlying mechanisms of the MCT-KD-induced improvement of DMD.

Heat Production and Energy Efficiency of Broilers Infected With Necrotic Enteritis.

Necrotic enteritis (NE) in poultry is the most important bacterial disease in terms of economic losses. The present study was conducted to evaluate the effect of an experimental challenge with necrotic enteritis on respiration and heat production in birds pretreated with dietary acylated starch or antibiotics (AB) zinc bacitracin (50 mg/kg) plus salinomycin (60 mg/kg). In total, 48 1-day-old Ross 308 male broilers were assigned to floor pens until day 10. On day 11, birds were randomly placed into 16 calorimetric chambers with four replicates of three birds per treatment. Treatments were: control, AB, acetylated high-amylose maize starch (SA), or butyrylated high-amylose maize starch (SB). Birds were NE challenged by inoculation with 5000 sporulated oocysts each of Eimeria maxima and Eimeria acervulina and 2500 sporulated oocysts of Eimeria brunetti on day 9 and Clostridium perfringens (3.8 × 10(8) colony-forming units) on day 14. The results showed that heat production (HP), respiratory quotient (RQ), heat increment, weight gain (WG), feed intake (FI), and livability (LV) of birds fed control, SA, and SB diets were lower than birds fed AB at 19 and 42 hr postinoculation (P < 0.05). At 65 hr postchallenge, increased FI and WG of birds were observed, indicating recovery from NE. During the entire period, from day 14 to day 17, birds fed control, SA, and SB had lower WG, FI, HP, RQ, metabolizable energy intake (MEI), and metabolizable energy (P < 0.01) than those fed AB. The data demonstrate that Eimeria sp. and C. perfringens challenge reduces growth performance, HP, RQ, metabolizable energy, and MEI of birds fed control, SA, and SB but not AB diets.

Dietary acylated starch improves performance and gut health in necrotic enteritis challenged broilers.

Resistant starch has been reported to act as a protective agent against pathogenic organisms in the gut and to encourage the proliferation of beneficial organisms. This study examined the efficacy of acetylated high amylose maize starch (SA) and butyralated high-amylose maize starch (SB) in reducing the severity of necrotic enteritis (NE) in broilers under experimental challenge. A total of 720 one-day-old male Ross 308 chicks were assigned to 48 floor pens with a 2 × 4 factorial arrangement of treatments. Factors were a) challenge: no or yes; and b) feed additive: control, antibiotics (AB), SA, or SB. Birds were challenged with Eimeria and C. perfringens according to a previously reported protocol. On d 24 and 35, challenged birds had lower (P < 0.001) livability (LV), weight gain (WG), and feed intake (FI) compared to unchallenged birds. Challenged birds fed SA and SB had higher FI and WG at d 24 and 35 (P < 0.05) compared to birds fed the control diet, while being significantly lower than those fed AB. Unchallenged birds fed SA or SB had higher FI at d 24 and 35 compared to those fed the control diet (P < 0.05). Birds fed SB had increased (P < 0.001) jejunal villus height/crypt depth (VH:CD) ratios at d 15, increased ileal (P < 0.001) and caecal (P < 0.001) butyrate levels at d 15 and 24, and decreased (P < 0.01) caecal pH at d 15. Birds fed SA had increased (P < 0.001) ileal acetate content at d 24 and decreased (P < 0.01) caecal pH at d 15. These results demonstrated that dietary acylated starch improved WG in birds challenged with necrotic enteritis. Depending on the acid used, starch acylation also offers a degree of specificity in short chain fatty acid (SCFA) delivery to the lower intestinal tract which improves gut health.

[A case of successful treatment of infected foot wound in the necrotic phase caused by allergic dermatitis using dietary supplement "Leiurus Arctica +"].

Clinical data of a single case of functional recovery and regeneration in pathologically altered foot tissue with extensive necrosis in during the course of therapy with the use of dietary supplement "Leiurus Arctica +" Clinical data indicates that the dietary supplement "Leiurus Arctica +" can be used as a wound healing agent.

Dietary lactose and its effect on the disease condition of necrotic enteritis.

Clostridium perfringens is the etiologic agent of necrotic enteritis (NE) and is ubiquitous in nature. The incidence of NE has increased in countries and commercial companies that have stopped using antibiotic growth promoters. The mechanisms of colonization of C. perfringens and the factors involved in onset of NE are not fully understood. Previously, our laboratory has demonstrated that lactose could potentially reduce Salmonella and C. perfringens in ceca of poultry. In the present investigation, we hypothesized that dietary lactose would reduce the clinical signs of NE and could be used as an alternative to antibiotics. In experiment 1, day-of-hatch broilers were fed either a nonlactose control diet, a diet with 2.5% lactose, or a diet with 4.5% lactose throughout the experiment. Birds were administered C. perfringens (10(7) cfu/mL) daily via oral gavage for 3 consecutive days starting on d 17. When evaluating the intestinal lesions associated with NE, birds fed 2.5% lactose had significantly lower (P < 0.05) lesion scores (0.70 +/- 0.52) compared with the control (1.55 +/- 0.52) or the 4.5% lactose (1.60 +/- 0.52). The data from the microbial analysis showed that the addition of lactose did not affect any bacterial populations when compared with the control birds that did not receive dietary lactose over the 21-d evaluation. The overall lesion scores in experiment 2 were significantly (P < 0.05) reduced in birds fed 2.5% lactose compared with the birds fed the control diet with mean lesion scores of 1.10 +/- 0.73 and 1.80 +/- 0.73, respectively. These experiments suggest that lactose could be used as a potential alternative to growth-promoting antibiotics to help control this costly disease.

Structural and functional changes after the administration of tetrachlormethane in the liver of rats fed on diets with different protein contents.

Morphological and biochemical changes characterizing the degree of liver damage and the development of liver repair were studied in rats fed 21 days on a low protein diet (LPD), a standard diet (SLD) and a high protein diet (HPD) and then given a single i.p. injection of tetrachlormethane (CCl4) in a dose of 0.75 ml/kg body weight. The HPD was found to increase sensitivity to CCl4, but it also promoted the liver repair process, as seen from the increment in liver DNA synthesis and the total DNA content of the liver, increased ploidy of the hepatocytes and growth of the size of their nuclei and of the hepatocytes themselves. An increase in the total surface area of the membranes of the granular endoplasmic reticulum and the inner and outer membrane of the mitochondria, but a decrease in the surface area of the membranes of the smooth endoplasmic reticulum, were also observed after the administration of CCl4. The LPD raised liver resistance to CCl4, but the development of liver repair activity differed from the process after the SLD and HPD, since polyploidy of the hepatocytes (especially the growth of octaploid cells) predominated and there was also an increase in the number of binuclear hepatocytes. Cell hypertrophy was expressed less in rats fed on the LPD than in animals given the HPD. As far as liver repair was concerned, the HPD showed no explicit advantages over the SLD.