Lars P. Kristensen

Bio: Lars P. Kristensen is an academic researcher from Odense University Hospital. The author has contributed to research in topics: Tenderness & Meat tenderness. The author has an hindex of 14, co-authored 22 publications receiving 860 citations. Previous affiliations of Lars P. Kristensen include University of Southern Denmark.

Dietary-induced changes of muscle growth rate in pigs: effects on in vivo and postmortem muscle proteolysis and meat quality.

Abstract: The effects of various growth rates in pigs induced by four different feeding strategies on the activity of the calpain system and on postmortem (PM) muscle proteolysis and tenderness development were studied. An increased growth rate may be caused by an increased protein turnover, which results in up-regulated levels of proteolytic enzymes in vivo that, in turn, possibly will affect PM tenderness development. It can be hypothesized that increased proteolytic activity pre-slaughter will increase the PM tenderization rate. From postnatal d 28 to d 90 (phase 1) the pigs were divided into two groups, given either ad libitum (A) or restricted (R, 60% of ad libitum) access to feed. The two groups were then divided into two subgroups, given either restricted or ad libitum access to feed from d 91 to slaughter at d 165 (phase 2). Measurements of the activity of mu-calpain, m-calpain, and calpastatin; concentrations of total collagen and the percent of soluble collagen; and RNA, DNA, and elongation factor-2 where made at slaugther. Myofibrillar fragmentation index (MFI) was determined at slaughter and 24 h PM. Warner-Braztler shear force was determined 1 d and 4 d PM. Pigs fed restricted diets in phase 1 and fed ad libitum in phase 2 (RA pigs) had increased growth rates in the last phase compared to pigs fed ad libitum during both phase 1 and phase 2 (AA pigs). The increased growth rate (compensatory growth) was followed by an increased proteolytic potential (mu-calpain:calpastatin ratio), increased MFI values, and higher tenderization rates. There was a positive correlation between the activities of m-calpain and growth rates (r = 0.35, P = 0.03), and between RNA levels and growth rates (r = 0.43, P = 0.006). The proposed hypothesis is largely supported by the results. The activities of both mu- and m-calpain at slaughter were highest in fast-growing pigs. The calpain activity was highest in RA pigs, which in turn also had the fastest growth rates prior tslaughter among the four groups. This implies that the synthesis of these enzymes was up-regulated during the second feeding period to a larger extent in RA pigs. The proteolytic potential and the MFI values indicate that the up-regulated in vivo calpain activity had an effect on PM protein degradation, which also is supported by the higher tenderization rate in RA pigs.

Compensatory growth response in pigs, muscle protein turn-over and meat texture: effects of restriction/realimentation period

Abstract: The present experiment was designed to evaluate the effect of different time spans of ad libitum feeding of pigs prior to slaughter after a period of restricted feeding on performance and texture characteristics of the meat. Te n litters of five pigs (Duroc ✕ Landrace ✕ Large White crosses) were allocated to five feeding treatments (AA, R28A42, R43A27, R52A18 and R60A10) at the age of 70 days. AA-pigs were given ad libitum a concentrate diet from day 70 to slaughter at day 140 (approx. 100 kg live weight). R28A42, R43A27, R52A18 and R60A10 pigs were given food at a restricted level (0·6 of ad libitum) for 28, 43, 52 and 60 days, respectively, followed by ad libitum feeding for 42, 27, 18 and 10 days, respectively, until slaughter at day 140. All pigs that had been given food at a restricted level for a period (R28A42, R43A27, R52A18 and R60A10) showed a compensatory growth response in the subsequent ad libitum period. However, only pigs on ad libitum for a minimum of 27 days prior to slaughter (R28A42 and R43A27) had carcass weights and muscle mass similar to that of the control pigs (AA) at slaughter. The restricted feeding increased meat proportion, whereas the feeding strategies had no effect on technological meat quality traits (pH24, drip loss and CIE-colour traits: L*, a* and b*). During compensatory growth, protein turn-over was increased and positively related to the length of the ad libitum period as indicated by the concentration of elongation factor-2 (eEF-2) (P < 0·10), the activity of µ-calpain (P < 0·01) and the myofibrillar fragmentation index (MFI) 1 day post mortem in m. longissimus dorsi (P < 0·08) and the solubility of collagen (P < 0·01). Although not significant, the shear force at day 1 followed the same pattern of improvement as the MFI. The concentration of eEF-2 increased at a faster rate following transition to ad libitum feeding than did the activity of µ-calpain. This suggests that muscle protein synthesis increases at a faster rate after change to ad libitum feeding and reaches the same level as in the control pigs (AA) before muscle protein degradation. This time lag between the increase in protein synthesis and degradation could explain the compensatory growth response and it also suggests that in order to use the compensatory growth mechanism to improve tenderness, the optimal time of slaughter may not coincide with the period of highest growth rates, but may occur at a later stage, when muscle protein degradation is maximal. For pigs slaughtered at 100 kg live weight, we expect muscle protein degradation to be maximal some time beyond 42 days of ad libitum feeding prior to slaughter.

Changes in the muscle proteome after compensatory growth in pigs.

Abstract: Sixteen female pigs (Duroc x Landrace x Large White) were divided into 2 groups, which had either free access to the diet (control group) or were feed-restricted from d 28 to 80 and then had free access to the diet (compensatory growth group). The sensory analysis showed that the pigs exhibiting compensatory growth produced meat with increased tenderness compared with control pigs (P < 0.05). To gain further knowledge of the influence of compensatory growth on meat tenderness, the sarcoplasmic protein fraction of muscle tissue was studied at the time of slaughter and 48 h postmortem using proteome analysis. At slaughter, 7 different proteins were found to be affected by compensatory growth: HSC70, HSP27, enolase 3, glycerol-3-phosphate dehydrogenase, aldehyde dehydrogenase E2, aldehyde dehydrogenase E3, and biphosphoglycerate mutase. The HSC70 and HSP27 both belong to the heat shock family and are known to play a role during muscle development. Hence, they may be affected by compensatory growth and increased protein turnover. Forty-eight hours after slaughter, 8 different proteins were found to be affected by compensatory growth: myosin light chain (MLC) II, MLC III, sulfite oxidase, chloride intracellular channel 1, 14-3-3 protein gamma, elongin B, and phosphohistidine phosphatase 14. The changes observed on MLC II and MLC III could be a consequence of enzymatic cleavage in the neck region of the globular myosin head domain that causes the release of MLC II and MLC III from the actomyosin complex. It has previously been hypothesized that compensatory growth results in an increased postmortem proteolysis; thus it was presumed that the intensity of some protein fragments would be affected by compensatory growth. However, the peptides that were found to be affected at 48 h postmortem were all full-length proteins. The 14-3-3 protein gamma has been proposed to play a role in the contraction of muscle during rigor and may thereby have an effect on meat tenderness. This study reveals some very interesting changes in the muscle proteome affected by compensatory growth, which may be useful in understanding the relationship among compensatory growth, protein turnover, and meat tenderness.

Compensatory growth improves meat tenderness in gilts but not in barrows

Abstract: Compensatory growth is a phenomenon observed in pigs given free access to feed following a period of restricted feeding that results in increased growth rates. Compensatory growth is believed to increase protein turnover and thereby the proteolytic potential at the time of slaughter, leading to faster tenderization rates of meat. Nine litters of three gilts and three barrows were allocated within litter and gender to three dietary treatment groups. Pigs had ad libitum access to feed from d 28 to slaughter at d 140 (ALA) or were restricted to 69% ad libitum from d 28 to d 80 or 90, and then given ad libitum access to the diet until slaughter at d 140 (RA80 and RA90, respectively). Pigs in the RA80 and RA90 treatment groups had a 9.7% higher (P < 0.001) fractional growth rate in the second feeding period than those in the ALA group. Growth rate was correlated to the activity of m-calpain (r = 0.37; P < 0.01), β-glucuronidase (r = 0.48; P < 0.001), and cathepsins B (r = 0.47; P < 0.001) and B+L (r = 0.31; P < 0.04). The LM of RA80-gilts received higher tenderness scores than the LM of ALA gilts, but tenderness scores were similar among barrows regardless of treatment (gender x treatment; P = 0.02). Conversely, tenderness scores were higher for the biceps femoris of ALA barrows than either ALA gilts or RA90 barrows (gender x treatment; P = 0.02). Desmin and troponin-T degradation, as well as myofibrillar fragmentation index, of the LM were not (P ≥ 0.24) affected by treatment. No dietary treatment effects were observed on the activities of μ-calpain (P = 0.15), m-calpain (P = 0.74), or calpastatin (P = 0.91) at slaughter. The cathepsin inhibitors, cystatins, tended to be increased (P = 0.06) in RA80 and RA90 pigs. Sarcomere length was longer (P = 0.003) in the LM of gilts than barrows. Barrows in the RA80 group had lower i.m. fat concentrations than ALA; however, no differences were found in the LM of gilts (gender x treatment; P = 0.03). The underlying hypothesis that compensatory growth leads to an increased proteolytic potential at the time of slaughter could not be verified in this study.

Lipid Oxidation in Oil-in-Water Emulsions: Impact of Molecular Environment on Chemical Reactions in Heterogeneous Food Systems

Abstract: The susceptibility of lipids to oxidation is a major cause of quality deterioration in food emulsions. The reaction mechanism and factors that influence oxidation are appreciably different for emulsified lipids than for bulk lipids. This article reviews the current understanding of the lipid oxidation mechanism in oil-in-water emulsions. It also discusses the major factors that influence the rate of lipid oxidation in emulsions, such as antioxidants, chelating agents, ingredient purity, ingredient partitioning, interfacial characteristics, droplet characteristics, and ingredient interactions. This knowledge is then used to define effective strategies for controlling lipid oxidation in food emulsions.

Antioxidant effectiveness as influenced by phenolic content of fresh orange juices.

Abstract: Several fresh orange juices, obtained from five different Citrus sinensis (L.) Osbeck varieties (three pigmented varieties, Moro, Sanguinello, and Tarocco, and two blond varieties, Valencia late and Washington navel), were subjected to antioxidant profile determination (including total polyphenols, flavanones, anthocyanins, hydroxycinnamic acids, and ascorbic acid). The antioxidant activity of these juices was then assessed by means of different “in vitro” tests (bleaching of the stable 1,1-diphenyl-2-picrylhydrazyl radical; peroxidation, induced by the water-soluble radical initiator 2,2‘-azobis(2-amidinopropane) hydrochloride, on mixed dipalmitoylphosphatidylcholine/linoleic acid unilamellar vesicles; scavenging activity against nitric oxide; total antioxidant status). All orange juices tested showed an evident antioxidant effect. Our findings indicate the following: (1) the antioxidant efficiency of orange juices may be attributed, in a significant part at least, to their content of total phenols, (2)...

Roles of Chk1 in cell biology and cancer therapy.

Abstract: The evolutionally conserved DNA damage response (DDR) and cell cycle checkpoints preserve genome integrity. Central to these genome surveillance pathways is a protein kinase, Chk1. DNA damage induces activation of Chk1, which then transduces the checkpoint signal and facilitates cell cycle arrest and DNA damage repair. Significant progress has been made recently toward our understanding of Chk1 regulation and its implications in cancer etiology and therapy. Specifically, a model that involves both spatiotemporal and conformational changes of proteins has been proposed for Chk1 activation. Further, emerging evidence suggests that Chk1 does not appear to be a tumor suppressor; instead, it promotes tumor growth and may contribute to anticancer therapy resistance. Recent data from our laboratory suggest that activating, but not inhibiting, Chk1 in the absence of chemotherapy might represent an innovative approach to suppress tumor growth. These findings suggest unique regulation of Chk1 in cell biology and cancer etiology, pointing to novel strategies for targeting Chk1 in cancer therapy.