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Research in growth and development, accumulation of lean, and fat metabolism in farm animals was gaining attention principally from a carcass perspective by meat scientists and animal nutritionists about a century ago. Under the auspices of the USDA Cooperative State Research Service, State Agricultural Experiment Stations, and the Land Grant University system, researchers from various universities embarked on forming combined regional research projects (across states) with unifying specific aims. In the North Central region, this included states in the upper and lower Mid-West region. For those interested in improving production and eating quality of meats, initially a single multistate committee was formed in the North Central region which was active for many years. However, these efforts were later split into two committees with one addressing lipids and the other muscle biology. Herein we reviewed research of workers in the North Central region in the 1940s and 1950s and to a limited extent in the 2000s on meat animal's lipid metabolism. We further reviewed the history of meat animal carcass composition research and the influence of the Word War II (WWII) period on porcine carcass composition. The development and utilization of adipocyte cellularity research methodology in meat animals was demonstrated. The history of the progression of adipose tissue metabolism research in meat animals was also reviewed. Finally, the history of research on lipid deposition in muscle that ultimately precipitated the expanded marbling and the intramuscular research was delineated. By the 1970s, great interest had emerged on how to curtail excessive fat deposition in meat-producing animals. Thus, for some segments of the animal lipid metabolism community, the focus then shifted to exploring the processes of lipogenesis and lipolysis in farm animals. These efforts morphed into research efforts in fat cell biology and cellularity. Today adipocyte biology is studied by many in the biomedical and agricultural-life sciences communities. In this article, we present a history of this research and notable achievements up to the 1980s. Herein we revisit these research efforts and results that have become an important knowledge base for growth and development, nutrition, and meat science research.

From a historical perspective, it is difficult to identify a specific date that launched the field of endocrinology. One "biomarker" of the inception of endocrinology traces back to Ernest Henry Starling, who first introduced the word hormone in a talk given in 1905 at the Royal College of Physicians in London (Starling, 1905). A historical look at the field of endocrine regulation of animal growth since 1905 conveys that countless scientists worldwide worked to advance the scientific evidence base, which led to the commercial development of hormone-based products that enhanced growth and beneficially changed carcass composition of meat animals. This review will discuss some of seminal contributions that include the discovery of hormones (like ST and beta-adrenergic agonists) that have been shown to play key roles in regulating growth and nutrient partitioning of livestock, the mechanisms by which these hormones act, and the development of products for application in animal agriculture.

Epidemiologic studies have consistently demonstrated beneficial effects of nut consumption on coronary heart disease (CHD) morbidity and mortality in different population groups. Clinical studies have reported total and low-density lipoprotein cholesterol-lowering effects of heart-healthy diets that contain various nuts or legume peanuts. It is evident that the favorable fatty acid profile of nuts (high in unsaturated fatty acids and low in saturated fatty acids) contributes to cholesterol lowering and, hence, CHD risk reduction. Dietary fiber and other bioactive constituents in nuts may confer additional cardioprotective effects.

Individual FA have diverse biological effects, some of which affect the risk of cardiovascular disease (CVD). In the context of food-based dietary guidance designed to reduce CVD risk, fat and FA recommendations focus on reducing saturated FA (SFA) and trans FA (TFA), and ensuring an adequate intake of unsaturated FA. Because stearic acid shares many physical properties with the other long-chain SFA but has different physiological effects, it is being evaluated as a substitute for TFA in food manufacturing. For stearic acid to become the primary replacement for TFA, it is essential that its physical properties and biological effects be well understood.

Alpha-linolenic acid (ALA) reduces cardiovascular disease (CVD) risk, possibly by favorably changing vascular inflammation and endothelial dysfunction. Inflammatory markers and lipids and lipoproteins were assessed in hypercholesterolemic subjects (n = 23) fed 2 diets low in saturated fat and cholesterol, and high in PUFA varying in ALA (ALA Diet) and linoleic acid (LA Diet) compared with an average American diet (AAD). The ALA Diet provided 17% energy from PUFA (10.5% LA; 6.5% ALA); the LA Diet provided 16.4% energy from PUFA (12.6% LA; 3.6% ALA); and the AAD provided 8.7% energy from PUFA (7.7% LA; 0.8% ALA). The ALA Diet decreased C-reactive protein (CRP, P < 0.01), whereas the LA Diet tended to decrease CRP (P = 0.08). Although the 2 high-PUFA diets similarly decreased intercellular cell adhesion molecule-1 vs. AAD (-19.1% by the ALA Diet, P < 0.01; -11.0% by the LA Diet, P < 0.01), the ALA Diet decreased vascular cell adhesion molecule-1 (VCAM-1, -15.6% vs. -3.1%, P < 0.01) and E-selectin (-14.6% vs. -8.1%, P < 0.01) more than the LA Diet. Changes in CRP and VCAM-1 were inversely associated with changes in serum eicosapentaenoic acid (EPA) (r = -0.496, P = 0.016; r = -0.418, P = 0.047), or EPA plus docosapentaenoic acid (r = -0.409, P = 0.053; r = -0.357, P = 0.091) after subjects consumed the ALA Diet. The 2 high-PUFA diets decreased serum total cholesterol, LDL cholesterol and triglycerides similarly (P < 0.05); the ALA Diet decreased HDL cholesterol and apolipoprotein AI compared with the AAD (P < 0.05). ALA appears to decrease CVD risk by inhibiting vascular inflammation and endothelial activation beyond its lipid-lowering effects.

We are transiting a time in which advances in plant molecular biology and genetics have resulted in a remarkable array of oils and fats that have a modified fatty acid profile, compared to the parent stock variety. The rapid evolution of modified oils and fats poses challenges for keeping nutrient databases current as well as deciphering what new fats/oils are used, from the standpoint of diet assessment and, in particular, collecting accurate dietary data. The expanding array of modified fats and oils has been designed to have greater shelf stability due to an increase in monounsaturated fat and enhanced health benefits due to a reduction in trans fat. The effects of oilseeds reduced in alpha-linolenic acid (ALA) on health outcomes need to be evaluated since diets rich in ALA have many health benefits.

"Bioactive compounds" are extranutritional constituents that typically occur in small quantities in foods. They are being intensively studied to evaluate their effects on health. The impetus sparking this scientific inquiry was the result of many epidemiologic studies that have shown protective effects of plant-based diets on cardiovascular disease (CVD) and cancer. Many bioactive compounds have been discovered. These compounds vary widely in chemical structure and function and are grouped accordingly. Phenolic compounds, including their subcategory, flavonoids, are present in all plants and have been studied extensively in cereals, legumes, nuts, olive oil, vegetables, fruits, tea, and red wine. Many phenolic compounds have antioxidant properties, and some studies have demonstrated favorable effects on thrombosis and tumorogenesis and promotion. Although some epidemiologic studies have reported protective associations between flavonoids or other phenolics and CVD and cancer, other studies have not found these associations. Various phytoestrogens are present in soy, but also in flaxseed oil, whole grains, fruits, and vegetables. They have antioxidant properties, and some studies demonstrated favorable effects on other CVD risk factors, and in animal and cell culture models of cancer. However, because phytoestrogens act both as partial estrogen agonists and antagonists, their effects on cancer are likely complex. Hydroxytyrosol, one of many phenolics in olives and olive oil, is a potent antioxidant. Resveratrol, found in nuts and red wine, has antioxidant, antithrombotic, and anti-inflammatory properties, and inhibits carcinogenesis. Lycopene, a potent antioxidant carotenoid in tomatoes and other fruits, is thought to protect against prostate and other cancers, and inhibits tumor cell growth in animals. Organosulfur compounds in garlic and onions, isothiocyanates in cruciferous vegetables, and monoterpenes in citrus fruits, cherries, and herbs have anticarcinogenic actions in experimental models, as well as cardioprotective effects. In summary, numerous bioactive compounds appear to have beneficial health effects. Much scientific research needs to be conducted before we can begin to make science-based dietary recommendations. Despite this, there is sufficient evidence to recommend consuming food sources rich in bioactive compounds. From a practical perspective, this translates to recommending a diet rich in a variety of fruits, vegetables, whole grains, legumes, oils, and nuts.

Oxidative modification of low density lipoprotein (LDL) is thought to play an important role in the development of atherosclerosis. Some studies have found that LDL enriched in monounsaturated fatty acids (MUFA) are less susceptible to oxidation than LDL enriched in polyunsaturated fatty acids (PUFA). A high MUFA diet is an alternative to a lower-fat blood cholesterol-lowering diet. Less is known about the effects of high MUFA versus lower-fat blood cholesterol-lowering diets on LDL oxidative susceptibility. The present study was designed to evaluate the effects of men and women consuming diets high in MUFA (peanuts plus peanut butter, peanut oil and olive oil) on LDL oxidative susceptibility, and to compare these effects with those of a Step II blood cholesterol-lowering diet. A randomized, double-blind, five-period crossover design (n = 20) was used to study the effects of the following diets on LDL-oxidation: average American [35% fat, 15% saturated fatty acids (SFA)], Step II (25% fat, 7% SFA), olive oil (35% fat, 7% SFA), peanut oil (35% fat, 7% SFA) and peanuts plus peanut butter (35% fat, 8% SFA). The average American diet resulted in the shortest lag time (57 +/- 6 min) for LDL oxidized ex vivo, whereas the Step II, olive oil and peanuts plus peanut butter diets resulted in a lag time of 66 +/- 6 min (P < or = 0.1). The slower rate of oxidation [nmol dienes/(min x mg LDL protein)] observed when subjects consumed the olive oil diet (24 +/- 2) versus the average American (28 +/- 2), peanut oil (28 +/- 2) and peanuts plus peanut butter diets (29 +/- 2; P < or = 0.05) was associated with a lower LDL PUFA content. The results of this study suggest that lower-fat and higher-fat blood cholesterol-lowering diets high in MUFA have similar effects on LDL oxidative resistance. In addition, our results suggest that different high MUFA sources varying in the ratio of MUFA to PUFA can be incorporated into a high MUFA diet without increasing the susceptibility of LDL to oxidation.

In the United States, intake of n-3 fatty acids is approximately 1.6 g/d ( approximately 0.7% of energy), of which 1.4 g is alpha-linolenic acid (ALA; 18:3) and 0.1-0.2 g is eicosapentaenoic acid (EPA; 20:5) and docosahexaenoic acid (DHA; 22:6). The primary sources of ALA are vegetable oils, principally soybean and canola. The predominant sources of EPA and DHA are fish and fish oils. Intake data indicate that the ratio of n-6 to n-3 fatty acids is approximately 9.8:1. Food disappearance data between 1985 and 1994 indicate that the ratio of n-6 to n-3 fatty acids has decreased from 12.4:1 to 10.6:1. This reflects a change in the profile of vegetable oils consumed and, in particular, an approximate 5.5-fold increase in canola oil use. The ratio of n-6 to n-3 fatty acids is still much higher than that recommended (ie, 2.3:1). Lower ratios increase endogenous conversion of ALA to EPA and DHA. Attaining the proposed recommended combined EPA and DHA intake of 0.65 g/d will require an approximately 4-fold increase in fish consumption in the United States. Alternative strategies, such as food enrichment and the use of biotechnology to manipulate the EPA and DHA as well as ALA contents of the food supply, will become increasingly important in increasing n-3 fatty acid intake in the US population.

Background: Low-fat diets increase plasma triacylglycerol and decrease HDL-cholesterol concentrations, thereby potentially adversely affecting cardiovascular disease (CVD) risk. High‐monounsaturated fatty acid (MUFA), cholesterol-lowering diets do not raise triacylglycerol or lower HDL cholesterol, but little is known about how peanut products, a rich source of MUFAs, affect CVD risk. Objective: The present study compared the CVD risk profile of an Average American diet (AAD) with those of 4 cholesterol-lowering diets: an American Heart Association/National Cholesterol Education Program Step II diet and 3 high-MUFA diets [olive oil (OO), peanut oil (PO), and peanuts and peanut butter (PPB)]. Design: A randomized, double-blind, 5-period crossover study design (n = 22) was used to examine the effects of the diets on serum lipids and lipoproteins: AAD [34% fat; 16% saturated fatty acids (SFAs), 11% MUFAs], Step II (25% fat; 7% SFAs, 12% MUFAs), OO (34% fat; 7% SFAs, 21% MUFAs), PO (34% fat; 7% SFAs, 17% MUFAs), and PPB (36% fat; 8% SFAs, 18% MUFAs). Results: The high-MUFA diets lowered total cholesterol by 10% and LDL cholesterol by 14%. This response was comparable with that observed for the Step II diet. Triacylglycerol concentrations were 13% lower in subjects consuming the high-MUFA diets and were 11% higher with the Step II diet than with the AAD. The high-MUFA diets did not lower HDL cholesterol whereas the Step II diet lowered it by 4% compared with the AAD. The OO, PO, and PPB diets decreased CVD risk by an estimated 25%, 16%, and 21%, respectively, whereas the Step II diet lowered CVD risk by 12%. Conclusion: A high-MUFA, cholesterol-lowering diet may be preferable to a low-fat diet because of more favorable effects on the CVD risk profile. Am J Clin Nutr 1999;70:1009‐15.

Background: Plasma lipid and lipoprotein responses have been variable in dietary intervention studies. Objective: The objective of this study was to evaluate the effects of the National Cholesterol Education Program's Step I and Step II dietary interventions on major cardiovascular disease risk factors using meta-analysis. Design: MEDLINE was used to select 37 dietary intervention studies in free-living subjects published from 1981 to 1997. Results: Step I and Step II dietary interventions significantly decreased plasma lipids and lipoproteins. Plasma total cholesterol (TC), LDL cholesterol, triacylglycerol, and TC:HDL cholesterol decreased by 0.63 mmol/L (10%), 0.49 mmol/L (12%), 0.17 mmol/L (8%), and 0.50 (10%), respectively, in Step I intervention studies, and by 0.81 mmol/L (13%), 0.65 mmol/L (16%), 0.19 mmol/L (8%), and 0.34 (7%), respectively, in Step II intervention studies (P < 0.01 for all). HDL cholesterol decreased by 7% (P = 0.05) in response to Step II but not to Step I dietary interventions. Positive correlations between changes in dietary total and saturated fatty acids and changes in TC and LDL and HDL cholesterol were observed (r = 0.59, 0.61, and 0.46, respectively: P

Etherton, Terry D., and Dale E. Bauman. Biology of Somatotropin in Growth and Lactation of Domestic Animals. Physiol. Rev. 78: 745–761, 1998. — Impressive progress has been made during the past 15 years in our understanding of the biology of somatotropin (ST) in domestic animals. In part, this progress was sparked by advances in biotechnology that made feasible the production of large quantities of recombinant bovine ST (bST) and porcine ST (pST). The availability of recombinant bST and pST resulted in an exponential increase in investigations that explored their role in growth and lactation biology, as well as evaluated their potential for commercial use. Collectively, these studies established that administration of bST to lactating dairy cows increased milk yield, and treatment of growing pigs with pST markedly stimulated muscle growth and reduced fat deposition. In addition to these “efficacy” studies, a substantial number of investigations examined the mechanisms by which ST affects lactation and growth of domestic animals. This review summarizes the diverse physiological effects ST has on growth and lactation and discusses the underlying mechanisms that mediate these effects in domestic animals.

A healthy eating pattern is recommended for the prevention and treatment of cardiovascular disease and overweight/obesity, two of the major chronic diseases that contribute to the global burden of diseases. The Mediterranean Diet, Dietary Approaches to Stop Hypertension Diet and, the US Department of Agriculture Food Patterns all meet current food-based and nutrient recommendations and can include lean beef. Lean beef is a nutrient-dense food and contains essential nutrients such as iron, zinc, and B-vitamins, as well as good-quality protein. Incorporating lean beef in a healthy dietary pattern would be expected to promote adherence to food-based dietary recommendations, achieve nutrient adequacy, and decrease risk of many major chronic diseases, notably cardiovascular disease and overweight/obesity.

Studies with animal models suggest that saturated fatty acids raise low density lipoprotein (LDL)-cholesterol levels by reducing LDL receptor-mediated clearance. To examine this directly in humans, we studied the effects of lowering dietary saturated fat on LDL-receptor abundance in peripheral mononuclear cells which reflects hepatic LDL-receptor status. Healthy males and females (n = 25) participating in the DELTA (Dietary Effects on Lipoproteins and Thrombogenic Activity) Study consumed three experimental diets in a randomized cross-over design. Diets provided 34% fat, 15% saturated fatty acids (Average American Diet); 29% fat, 9% saturated fatty acids (Step-One Diet); and 25% fat, 6% saturated fatty acids (Low SAT Diet). Peripheral mononuclear cells were isolated from blood samples collected after 6 and 8 wk. An ELISA was used to quantify LDL-receptor protein in total cell membranes. LDL-receptor abundance increased by 10.5% after the Low SAT Diet (P < 0.05). This was associated with an 11.8% decrease in serum LDL-cholesterol (P < 0.05). A linear inverse relationship was observed between the percentage change in LDL-cholesterol and the percentage change in LDL-receptor abundance (r = -0.59; P < 0.01). In addition, LDL-receptor abundance also was correlated inversely (P < 0.001) with serum levels of LDL-cholesterol (r = -0.747) and apoB (r = -0.593). In summary, reducing dietary saturated fat is associated with an increase in LDL-receptor abundance of magnitude similar to the decrease in serum LDL-cholesterol. Thus, an important mechanism by which reductions in dietary saturated fatty acids decrease LDL-cholesterol in humans is through an increase in LDL-receptor number.

Background The erythrocyte membrane content of eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ), which constitutes the omega‐3 index (O3I), predicts cardiovascular disease mortality. The amount of EPA + DHA needed to achieve a target O3I is poorly defined, as are the determinants of the O3I response to a change in EPA + DHA intake. The objective of this study was to develop a predictive model of the O3I response to EPA + DHA supplementation in healthy adults, specifically identifying factors that determine the response. Methods and Results A randomized, placebo‐controlled, double‐blind, parallel‐group study was conducted in 115 healthy men and women. One of 5 doses (0, 300, 600, 900, 1800 mg) of EPA + DHA was given daily as placebo or fish oil supplements for ≈5 months. The O3I was measured at baseline and at the end of the study. There were no significant differences in the clinical characteristics between the groups at baseline. The O3I increased in a dose‐dependent manner ( P EPA + DHA alone accounting for 68% (quadratic, P P P Conclusions Our findings validate the O3I as a biomarker of EPA + DHA consumption and identify additional factors, particularly body weight, that can be used to tailor EPA + DHA recommendations to achieve a target O3I.

The present study was conducted to determine the effects of dietary fatty acids on hepatic LDL receptor (LDLr) protein abundance and mRNA levels. Sixty pigs were randomized into 10 groups and fed corn-soybean meal diets containing three cholesterol levels (0.25%, 0.5%, and 1.0%, w/w) with no added fat, or fats rich (30% of calories) in palmitic acid or linoleic acid. A control group was fed the base diet with no added fat. After 30 days, plasma LDL-cholesterol (LDL-C) levels increased as the dietary cholesterol increased (P < 0.05); however, there was no significant effect of either fatty acid. Dietary fatty acids, however, had distinctly different effects on hepatic LDLr protein (analyzed by ELISA) and mRNA (analyzed by Northern blot) abundance. When pigs consumed diets containing 0.25% cholesterol, linoleic acid increased hepatic LDLr protein 40% whereas palmitic acid reduced it 40% (P < 0.05). These changes in LDLr protein abundance were accompanied by parallel changes in hepatic LDLr mRNA; linoleic acid increased LDLr mRNA 2-fold (P < 0.01), whereas palmitic acid decreased it 60% (P < 0.01). The differential effects of fatty acids on LDLr expression were only observed at 0.25% cholesterol, suggesting that higher intakes of cholesterol have a dominant and repressive effect on regulation of LDLr expression. Cholesterol intake increased hepatic total cholesterol levels (P < 0.01) while dietary fatty acids had no effect on hepatic sterols. In summary, our results indicate that dietary linoleic acid and palmitic acid have markedly different effects on hepatic LDLr protein abundance that are mediated by differential effects on LDLr mRNA and protein levels. Further studies are needed to fully elucidate the molecular mechanisms by which fatty acids regulate LDLr mRNA and protein levels.

International audience; The present study was conducted to determine whether porcine somatotropin (pST) differentially regulates expression of the GLUT4 and fatty acid synthase (FAS) genes in pig adipose tissue. Three different experiments were conducted in which pigs were treated daily with different doses of pST for different time periods (7 or 14 d and from 60 to 90 kg of body wt). In these experiments, pST significantly and consistently decreased FAS mRNA levels (80%, 66% and 85%, respectively); however, GLUT4 mRNA was not affected by pST in two of the three experiments, and in the one showing an effect (Experiment 2), the decrease was less than observed for FAS (44%). Because of these results, we conducted subsequent experiments to see if the effects of pST on glucose metabolism in cultured pig adipose tissue (48 h) differed when glucose concentrations were changed from 1 to 5 mmol/L. These studies revealed that the antagonistic effect of pST on insulin action was more potent when glucose transport was saturated (5 mmol/L) than when glucose concentration limited glucose entry into the cell (1 mmol/L). In summary, these results suggest that the effects of pST on glucose transport in pig adipocytes are secondary to changes elicited by the hormone on intracellular glucose use for lipogenesis. When considered in the context of the decrease previously observed in glucose transport in pig adipocytes, the findings reported herein suggest that pST acts to decrease GLUT4 protein activity and/or distribution between the plasma membrane and the intracellular pool with little alteration in GLUT4 gene expression or total cell GLUT4 protein.

The present study was conducted to determine the chronic effects of porcine growth hormone administration on fatty acid synthase (FAS) mRNA abundance and gene transcription in growing rats. Growth hormone treatment increased growth rate approximately 27% (P

In the present study we used regression analyses to evaluate the effects of stearic acid (18:0) on total cholesterol (TC), low-density-lipoprotein-cholesterol (LDL-C), and high-density-lipoprotein-cholesterol (HDL-C) concentrations (mmol/L). Using data from 18 articles, we developed the following predictive equations (monounsaturated fatty acids, MUFAs; polyunsaturated fatty acids, PUFAs): delta TC = 0.0522 delta 12:0-16:0 - 0.0008 delta 18:0 - 0.0124 delta MUFA - 0.0248 delta PUFA; delta LDL-C = 0.0378 delta 12:0-16:0 + 0.0018 delta 18:0 - 0.0178 delta MUFA - 0.0248 delta PUFA; delta HDL-C = 0.0160 delta 12:0-16:0 - 0.0016 delta 18:0 + 0.0101 delta MUFA + 0.0062 delta PUFA. Our analyses revealed that unlike the other long-chain saturated fatty acids (SFAs), stearic acid had no effect on TC and lipoprotein cholesterol concentrations in men and women. MUFAs elicited an independent hypocholesterolemic effect that we believe is due to the small amount of 12:0-16:0 in the experimental diets evaluated. The observation that stearic acid has unique effects on TC, LDL-C, and HDL-C provides additional compelling evidence that it be distinguished from the other major SFAs in blood cholesterol predictive equations.

The present study was undertaken to investigate the effects of porcine IGFBP-3 on IGF-I stimulated DNA synthesis in neonatal porcine skin fibroblasts. IGF-1 stimulated DNA synthesis in skin fibroblasts in a concentration dependent manner. DNA synthesis was maximally stimulated by 5 to 20 fold at 5 nM IGF-I; half-maximal stimulation was observed at approximately 1 nM IGF-I. Co-incubation of IGFBP-3 with a maximally effective dose of IGF-I (10 nM) did not inhibit the stimulatory effects of IGF-I on DNA synthesis. In contrast, when IGFBP-3 at concentrations of 0 to 20 nM was co-incubated with 1 nM IGF-I, a bi-phasic dose response was observed with IGFBP-3 being inhibitory only at a 10 to 20 fold molar excess to IGF-I. Based on the approximately equal molar ratio of IGFBP-3:IGF-I present in the circulation of control and pST-treated pigs our results suggest that IGFBP-3 does not inhibit the mitogenic effects of IGF-I. In summary, these results indicate that the combination of IGFBP-3 with IGF-I optimizes mitogenic signalling via the type I IGF receptor and suggest that IGFBP-3 does not inhibit the effects of ST that are mediated by IGF-I.

With the approval of bST for use in enhancing productive efficiency and milk production of dairy cows the public has been subjected to confusing public discussions about the health consequences of using biotechnology to improve our food supply. This paper presents a scientist's assessment of its effect on animal agriculture and the consumer.

Plasma lipids, lipoproteins, and apolipoproteins were measured in 123 female and 57 male Mvskoke Indians, a population of American Indians with a high prevalence of non-insulin-dependent diabetes mellitus (NIDDM). Dietary patterns were assessed with a food-frequency questionnaire. There were no differences in total cholesterol, low-density-lipoprotein cholesterol (LDL-C), high-density-lipoprotein cholesterol (HDL-C), apolipoproteins A-I or B in female Indians with and without diabetes. In males with diabetes, however, LDL-C was lower. Triglyceride and fasting plasma glucose were higher in subjects with diabetes. Total cholesterol and LDL-C were lower and HDL-C was higher than age and sex-matched Lipid Research Clinics values, especially for subjects with diabetes. This is surprising given that the diet of Mvskoke Indians contains foods high in total fat, saturated fatty acids, and cholesterol. We may explain, in part, the low incidence of coronary heart disease in this population.

When growing pigs are treated daily with recombinantly derived porcine somatotropin (pST) for 30-60 d there is a dose-dependent decrease in lipid accretion. Maximal doses of pST can reduce lipid accretion by as much as 70%. The reduction in lipid accretion occurs because of a marked decrease in glucose transport and lipogenesis that is the result of a pST-dependent decrease in the ability of insulin to stimulate these processes in the adipocyte; lipolysis is not affected. The decrease in insulin sensitivity is not due to a decrease in insulin binding or insulin receptor kinase activity. Little is understood about the somatotropin (ST) intracellular signal pathway(s) that mediate the biological effects of ST. These effects are chronic rather than acute as was previously believed. This pattern likely reflects that ST decreases transcription of important insulin-responsive genes such as the muscle-adipose tissue transporter gene (GLUT4) and key lipogenic enzymes.

During the past 20 years, much has been learned about how porcine somatotropin (pST) affects growth and nutrient partitioning in growing pigs. The development of techniques to produce large quantities of recombinantly de- rived pST enabled numerous long-term studies to be con- ducted in which the effects of daily pST administration could be evaluated. Collectively, these studies established that treatment of growing pigs with pST markedly stimulated mus- cle growth and, concurrently, reduced fat deposition. In grow- ing pigs, maximally effective doses of pST increase average daily gain as much as 10-20%, improve feed efficiency 15- 30%, decrease adipose tissue mass and lipid accretion rates by as much as 50-80% and concurrently increase protein deposition by 50%. These effects are associated with a de- crease in feed intake of ;10-15%. These responses occur because pST has a wide array of biological effects that mod- ulate nutrient partitioning between adipose tissue and skele- tal muscle. The decrease in adipose tissue growth is due to a reduction in lipogenesis that is the consequence of pST blunt- ing the effects of many insulin-dependent events. With re- spect to fatty acid synthase (FAS), a pace-setting enzyme in the lipogenic pathway, enzyme activity is markedly reduced by pST. This is the result of a pST-mediated decrease in FAS mRNA levels that occurs because FAS gene transcription is decreased. The consequence of the decrease in lipid synthe- sis is that adipocyte hypertrophy is impaired and, hence, tis- sue growth. This review will provide an overview of some of the biological effects of pST in adipose tissue and will discuss what is known about the underlying mechanisms that ac- count for these effects. J. Nutr. 130: 2623-2625, 2000.

Various organizations worldwide have made dietary recommendations for eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and fish intake that are primarily for coronary disease risk reduction and triglyceride (TG) lowering. Recommendations also have been made for DHA intake for pregnant women, infants, and vegetarians/vegans. A Dietary Reference Intake (DRI), specifically, an Adequate Intake (AI), has been set for α-linolenic acid (ALA) by the Institute of Medicine (IOM) of The National Academies. This amount is based on an intake that supports normal growth and neural development and results in no nutrient deficiency. Although there is no DRI for EPA and DHA, the National Academies have recommended that approximately 10% of the Acceptable Macronutrient Distribution Range (AMDR) for ALA can be consumed as EPA and/or DHA. This recommendation represents current mean intake for EPA and DHA in the United States (≈100 mg/day), which is much lower than what many groups worldwide are currently recommending. Global recommendations for long-chain omega-3 fatty acids underscore the pressing need to establish DRIs for DHA and EPA because DRIs are recognized as the “official” standard by which federal agencies issue dietary guidance or policy directives for the health and well-being of individuals in the United States and Canada. Because of the many health benefits of DHA and EPA, it is important and timely that the National Academies establish DRIs for the individual long-chain (20 carbons or greater) omega-3 fatty acids. Refereed/Peer-reviewed

Using competitive ligand-binding studies, ligand blotting, and immunoprecipitation, we have characterized the insulin-like growth factor (IGF)-binding proteins (BPs) of porcine follicular fluid. Competitive ligand-binding studies revealed a preference of ovarian IGFBPs for IGF-II over IGF-I. Follicular fluid from small, 1-3-mm follicles had nearly twice the binding capacity for IGFs as that from large, 6-10-mm follicles. Ligand blots of porcine follicular fluid resolved 5 major bands of IGF-binding activity having apparent molecular sizes of 44, 40, 34, 29, and 22 kDa. The 40-44-kDa bands were immunoprecipitated by an antibody to porcine IGFBP-3, the acid-stable subunit of the 150-kDa growth hormone-dependent IGF-binding protein complex of porcine serum. The 34-kDa band was immunoprecipitated by an antibody to rat IGFBP-2, the major IGF-binding protein found in fetal rat serum. To date we have been unable to immunoprecipitate the 29- and 22-kDa bands with any of the antibodies tested, including a panel of monoclonal antibodies to human IGFBP-1, the amniotic fluid IGF-binding protein. The 40-44-kDa species (IGFBP-3) was the predominant form and was equally abundant in fluid from large and small follicles. In contrast, the smaller forms, including IGFBP-2 and the 29- and 22-kDa forms were significantly more prominent in fluid from small follicles. In view of other studies indicating a significant effect of IGFBPs on ovarian cell function, follicular IGFBPs may play an important role in the IGF autocrine/paracrine regulatory system of the ovary.

A trend in food labeling is to make claims related to agricultural management, and this is occurring with dairy labels. A survey study was conducted to compare retail milk for quality (antibiotics and bacterial counts), nutritional value (fat, protein, and solids-not-fat), and hormonal composition (somatotropin, insulin-like growth factor-1 [IGF-1], estradiol, and progesterone) as affected by three label claims related to dairy-cow management: conventional, recombinant bovine somatotropin (rbST)-free (processor-certified not from cows supplemented with rbST), or organic (follows US Department of Agriculture organic practices). Retail milk samples (n=334) from 48 states were collected. Based on a statistical analysis that reflected the sampling schema and distributions appropriate to the various response variables, minor differences were observed for conventional, rbST-free, and organic milk labels. Conventionally labeled milk had the lowest (P

BACKGROUND: Atherosclerosis is a chronic inflammatory disease. We previously reported that a diet high in alpha-linolenic acid (ALA) reduces lipid and inflammatory cardiovascular disease risk factors in hypercholesterolemic subjects. OBJECTIVE: The objective was to evaluate the effects of a diet high in ALA on serum proinflammatory cytokine concentrations and cytokine production by cultured peripheral blood mononuclear cells (PBMCs) from subjects fed the experimental diets. DESIGN: A randomized, controlled, 3-diet, 3-period crossover study design was used. Hypercholesterolemic subjects (n = 23) were assigned to 3 experimental diets: a diet high in ALA (ALA diet; 6.5% of energy), a diet high in linoleic acid (LA diet; 12.6% of energy), and an average American diet (AAD) for 6 wk. Serum interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha (TNF-alpha) concentrations and the production of IL-6, IL-1beta, and TNF-alpha by PBMCs were measured. RESULTS: IL-6, IL-1beta, and TNF-alpha production by PBMCs and serum TNF-alpha concentrations were lower (P < 0.05 and P < 0.08, respectively) with the ALA diet than with the LA diet or AAD. PBMC production of TNF-alpha was inversely correlated with ALA (r = -0.402, P = 0.07) and with eicosapentaenoic acid (r = -0.476, P = 0.03) concentrations in PBMC lipids with the ALA diet. Changes in serum ALA were inversely correlated with changes in TNF-alpha produced by PBMCs (r = -0.423, P < 0.05). CONCLUSIONS: Increased intakes of dietary ALA elicit antiinflammatory effects by inhibiting IL-6, IL-1beta, and TNF-alpha production in cultured PBMCs. Changes in PBMC ALA and eicosapentaenoic acid (derived from dietary ALA) are associated with beneficial changes in TNF-alpha release. Thus, the cardioprotective effects of ALA are mediated in part by a reduction in the production of inflammatory cytokines.

The objective of this study was to investigate the effect of individual PUFAs on LDL receptor (LDLr) expression in human fibroblasts and HepG2 cells, and to evaluate whether acyl CoA:cholesterol acyltransferase (ACAT) and sterol regulatory element-binding protein 1 (SREBP-1) were involved in the regulation of LDLr expression by fatty acids. When fibroblasts and HepG2 cells were cultured with serum-free defined medium for 48 h, there was a 3- to 5-fold (P 0.05) increase in LDLr protein and mRNA levels. Incubation of fibroblasts and HepG2 cells in serum-free medium supplemented with 25-hydroxycholesterol (25OH-cholesterol, 5 mg/L) for 24 h decreased LDLr protein and mRNA levels by 50 -90% (P 0.05). Arachidonic acid (AA, 20:4(n-6)), EPA (20:5(n-3)), and DHA (22:6(n-3)) antagonized the depression of LDLr gene expression by 25OH-cholesterol and increased LDLr protein abundance 1- to 3-fold (P 0.05), but had no significant effects on LDLr mRNA levels. Oleic (18:1), linoleic (18:2), and -linolenic acids (18:3(n-3)) did not significantly affect LDLr expression. ACAT inhibitor (58 - 035, 1 mg/L) attenuated the regulatory effect of AA on LDLr protein abundance by 40% (P 0.05), but did not modify the regulatory effects of other unsaturated fatty acids in HepG2 cells. The present results suggest that AA, EPA, and DHA increase LDLr protein levels, and that ACAT plays a role in modulating the effects of AA on LDLr protein levels. Furthermore, the effects of the fatty acids appeared to be independent of any change in SREBP-1 protein. J. Nutr. 135: 2541-2545, 2005.

The effects of linoleic acid (LA), alpha-linolenic acid (ALA), and docosahexaenoic acid (DHA) were compared to that of palmitic acid (PA), on inflammatory responses in human monocytic THP-1 cells. When cells were pre-incubated with fatty acids for 2-h and then stimulated with lipopolysaccharide for 24-h in the presence of fatty acids, secretion of interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha (TNFalpha) was significantly decreased after treatment with LA, ALA, and DHA versus PA (P < 0.01 for all); ALA and DHA elicited more favorable effects. These effects were comparable to those for 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2) and were dose-dependent. In addition, LA, ALA, and DHA decreased IL-6, IL-1beta, and TNFalpha gene expression (P < 0.05 for all) and nuclear factor (NF)-kappaB DNA-binding activity, whereas peroxisome proliferator-activated receptor-gamma (PPARgamma) DNA-binding activity was increased. The results indicate that the anti-inflammatory effects of polyunsaturated fatty acids may be, in part, due to the inhibition of NF-kappaB activation via activation of PPARgamma.

▪ Abstract Identifying bioactive compounds and establishing their health effects are active areas of scientific inquiry. There are exciting prospects that select bioactive compounds will reduce the risk of many diseases, including chronic diseases such as cardiovascular disease. Recent findings have established that cardiovascular disease is a disease of inflammation, and consequently is amenable to intervention via molecules that have anti-inflammatory effects. In addition, research demonstrating adverse effects of oxidants on atherogenesis raises the possibility that antioxidants can confer cardioprotective effects. This review provides an overview of research approaches that can be used to unravel the biology and health effects of bioactive compounds. Because of the number of bioactive compounds and the diversity of likely biological effects, numerous and diverse experimental approaches must be taken to increase our understanding of the biology of bioactive compounds. Recognizing the complexity of this biology, sophisticated experimental designs and analytical methodologies must be employed to advance the field. The discovery of novel health effects of bioactive compounds will provide the scientific basis for future efforts to use biotechnology to modify/fortify foods and food components as a means to improve public health.

Conjugated linoleic acid (CLA) exerts anticarcinogenic and antiatherosclerotic effects in animals. The present study was conducted to examine the effects of CLA on LDL receptor (LDLr) expression in HepG2 cells, and to evaluate whether the sterol response element binding protein 1 (SREBP-1) and acyl CoA:cholesterol acyltransferase (ACAT) were involved in the regulation of LDLr expression by CLA. When HepG2 cells were cultured with serum-free DMEM for 48 h, there was a three- to fivefold (P

For the first time, Dietary Reference Intakes (DRIs) for macronutrients have been established by the National Academies’ Institute of Medicine for the United States and Canada (1). This science-based report makes new recommendations for energy, carbohydrates, fiber, fat, fatty acids, cholesterol, protein, and amino acids. The DRI Report embraces the philosophy of making dietary recommendations that assure a nutritionally adequate diet, promote good health, prevent chronic disease, and avoid overconsumption. Recommendations suggest that adults should consume a diet that provides 45% to 65% of their calories from carbohydrates, 10% to 35% from protein, and 20% to 35% from fat. The report advises that saturated fat, trans fat, and cholesterol be as low as possible. Because polyunsaturated fatty acids (PUFAs) are essential nutrients, the DRI Report recommends 17 g/d for men and 12 g/d for women of linoleic acid (C 18:2), an omega-6 PUFA. For cs-linolenic acid (ALA), an omega-3 fatty acid, 1.6 and 1.1 g/d should be consumed by men and women, respectively. The recommendations for PUFA are based on average intakes in the United States. For simplicity, the report recommends that 5% to 10% of calories come from PUFA and 0.6% to 1.2% come from ALA. Importantly, approx 10% of omega-3 fatty acid intake can come from long-chain, highly unsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Because of the total fat recommendation and the guidance provided about saturated fat, trans fat, and PUFA intake, the balance will be derived from monounsaturated fatty acids (MUFAs). The range of total fat from 20% to 35% of calories recognizes that healthy diets can be planned over a reasonably broad range of fat intake, as long as saturated fat, trans fat, and cholesterol are kept as low as possible. This range in total fat reflects the health benefits of unsaturated fat in the context of a nutritionally adequate diet that promotes a healthy weight. The range of all macronutrients acknowledges that there are many healthy diets with respect to macronutrient profiles, as long as each diet meets the specific recommendations made in the DRI Report for saturated fat, trans fat, cholesterol, total fiber (38 g/d for men and 25 g/d for women), and added sugar (a maximum of 25% or fewer calories from added sugars).

Purpose of review To discuss new evidence-based dietary recommendations founded on an inclusive food strategy and to address the challenges that are posed by integrating a growing list of heart healthy foods into the diet without increasing energy intake beyond that required to achieve a healthy body weight. Recent findings New food-based dietary recommendations issued by the American Heart Association with the objective of reducing risk for cardiovascular disease (CVD) promote an inclusionary approach. The American Heart Association recommends a variety of foods to target four major goals: achieve a healthy overall diet, achieve a healthy weight, promote desirable lipid levels, and promote desirable blood pressure. Specific foods recommended include fruits and vegetables, grain products (including whole grains), fish, lean meat and poultry, fat-free or low-fat dairy products, and legumes. In addition, the new National Cholesterol Education Program Adult Treatment Panel III recommends reductions in saturated fat and cholesterol and therapeutic dietary options for enhancing LDL-cholesterol lowering, with inclusion of plant stanols/sterols (2 g/day) and increased viscous (soluble) fiber (10-25 g/day). In parallel with the evolution of new dietary recommendations is the expanding list of specific foods that have cardioprotective effects. Additional foods on this list are nuts, soy, legumes, alcohol, tea, and garlic. Summary It will be challenging to include all foods that reduce CVD risk in the diet and still maintain energy control. Strategies are needed that facilitate developing heart healthy dietary patterns that maximally reduce CVD risk.

Background Flavonoids are polyphenolic compounds of plant origin with antioxidant effects. Flavonoids inhibit LDL oxidation and reduce thrombotic tendency in vitro. Little is known about how cocoa powder and dark chocolate, rich sources of polyphenols, affect these cardiovascular disease risk factors. Objective We evaluated the effects of a diet high in cocoa powder and dark chocolate (CP-DC diet) on LDL oxidative susceptibility, serum total antioxidant capacity, and urinary prostaglandin concentrations. Design We conducted a randomized, 2-period, crossover study in 23 healthy subjects fed 2 diets: an average American diet (AAD) controlled for fiber, caffeine, and theobromine and an AAD supplemented with 22 g cocoa powder and 16 g dark chocolate (CP-DC diet), providing approximately 466 mg procyanidins/d. Results LDL oxidation lag time was approximately 8% greater (P = 0.01) after the CP-DC diet than after the AAD. Serum total antioxidant capacity measured by oxygen radical absorbance capacity was approximately 4% greater (P = 0.04) after the CP-DC diet than after the AAD and was positively correlated with LDL oxidation lag time (r = 0.32, P = 0.03). HDL cholesterol was 4% greater after the CP-DC diet (P = 0.02) than after the AAD; however, LDL-HDL ratios were not significantly different. Twenty-four-hour urinary excretion of thromboxane B(2) and 6-keto-prostaglandin F(1)(alpha) and the ratio of the 2 compounds were not significantly different between the 2 diets. Conclusion Cocoa powder and dark chocolate may favorably affect cardiovascular disease risk status by modestly reducing LDL oxidation susceptibility, increasing serum total antioxidant capacity and HDL-cholesterol concentrations, and not adversely affecting prostaglandins.

During the past 20 y, much has been learned about how porcine growth hormone (pGH) affects growth and nutrient partitioning in growing pigs. Our contemporary understanding of the biology of pGH has as its roots the seminal studies conducted by Larry Machlin. His studies and many subsequent reports by other investigators have established that treatment of growing pigs with pGH markedly stimulates muscle growth and, concurrently, reduces fat deposition. In growing pigs, maximally effective doses of pGH increase average daily gain as much as 10% to 20%, improve feed efficiency 15% to 30%, decrease adipose tissue mass and lipid accretion rates by as much as 50% to 80%, and concurrently increase protein deposition by 50%. These effects are associated with a decrease in feed intake of approximately 10% to 15%. These responses occur because pGH has a wide array of biological effects that modulate nutrient partitioning between adipose tissue and skeletal muscle. The decrease in adipose tissue growth is due to a reduction in lipogenesis that is the consequence of pGH blunting the effects of many insulin-dependent events. This article provides an overview of some of the biological effects pGH has in adipose tissue and discusses what is known about the underlying mechanisms that account for these effects.

The present study examined the effects of reducing dietary total fat and saturated fat (SFA) on LDL oxidative susceptibility in 27 healthy men and women (age 24-65 y). Each subject consumed each of three diets for 8 wk: an average American diet (AAD, 34% energy from fat, 15% from SFA), a Step-1 diet (29% fat, 9% SFA) and a very low SFA diet (Low-Sat, 25% fat, 6% SFA). In vitro LDL oxidation was assessed by copper-mediated oxidation, as measured by the kinetics of conjugated diene formation and lipid peroxide formation. Compared with the AAD, plasma LDL-cholesterol (LDL-C) and HDL cholesterol levels were 8% lower (P: = 0.16 and P: = 0.11, respectively), in subjects when they consumed the Step-1 diet and 11% (P: < 0.03) and 14% (P: < 0.057) lower, respectively, when they consumed the Low-Sat diet. Conjugated diene production and oxidation rate were 7% (P: < 0. 05) and 9% (P: < 0.05) lower, respectively. The reduction of lipid peroxide formation was 9% (P: < 0.05) in subjects when they consumed the Low-Sat diet vs. the AAD. In addition, lipid peroxide and conjugated diene formation were positively correlated with plasma total and LDL-C and apolipoprotein B (apo B) levels (r = 0.5-0.6, P: < 0.001), suggesting that quantity of LDL is an important determinant of oxidative modification. Furthermore, at the same level of apo B or LDL-C, LDL from subjects when they consumed either Step-1 or Low-Sat diets was less susceptible (P: < 0.05) to oxidation than those when they consumed the AAD, suggesting that qualitative changes also affect LDL oxidative susceptibility. Therefore, the benefits of lowering dietary SFA may extend beyond decreasing LDL-C levels and include favorable qualitative changes in LDL that further decrease risk of coronary heart disease.

Somatotropin (ST) markedly decreases lipogenesis, fatty acid synthase (FAS) enzyme activity and mRNA abundance in pig adipocytes. The present study was conducted to determine whether the decrease in FAS mRNA in 3T3-F442A adipocytes was the result of a decrease in transcription of the FAS gene and/or a change in FAS mRNA stability. Insulin increased the abundance of FAS mRNA 2–13-fold and fatty acid synthesis 3–7-fold. Somatotropin decreased the stimulatory effect of insulin on the abundance of FAS mRNA and lipogenesis by 40–70% and 20–60% respectively. Subsequent run-on analyses demonstrated that the decrease observed in FAS mRNA in response to ST was associated with an 82% decrease in transcription; ST significantly shortened the half-life of FAS mRNA from 35 to 11 h. To corroborate the run-on analyses, cells were stably transfected with a pFAS–CAT5 (in which CAT stands for chloramphenicol acetyltransferase) reporter construct that contained 2195 bp of the 5´ flanking region of the rat FAS gene. Insulin treatment increased FAS–CAT activity 4.7-fold. When ST was added to the insulin-containing medium there was an approx. 60% reduction in FAS–CAT activity. In summary, our results indicate that ST decreases FAS mRNA levels and that this is the result of a marked decrease in both transcription of the FAS gene and stability of the FAS mRNA.

A 246-bp fragment of porcine glucose transporter 4 (GLUT4) cDNA was cloned by polymerase chain reaction (PCR) from porcine adipose tissue RNA. Nucleotide sequences 1-138 and 139-246 of the GLUT4 cDNA share 78% sequence identity with exon 4a and 91% sequence identity with exon 4b of the human GLUT4 gene, respectively. The GLUT4 cDNA fragment was subcloned into pGEM-4Z vector to synthesize a highly specific riboprobe that hybridized only to human GLUT4 cDNA but not to human glucose transporter 1 (GLUT1) cDNA. Northern blot analysis of total RNA revealed the presence of a single transcript of 2.8 kb in porcine adipose tissue. Cloning a fragment of the GLUT4 cDNA enabled us to develop a ribonuclease protection assay for detecting porcine GLUT4 mRNA. The ribonuclease (RNase) protection assay is highly reproducible and retains a sensitivity level to as little as 2 pg of GLUT4 mRNA. The standard curve was linear between 2 and 128 pg of sense-strand GLUT4 RNA (r = .994). The ability to detect small quantities of GLUT4 mRNA is important when the abundance of GLUT4 mRNA is low and the quantity of tissue is limiting (e.g., when RNA is extracted from cultured adipose tissue). When porcine adipose tissue explants were cultured in the presence of insulin (10 ng/mL), GLUT4 mRNA abundance was increased. Development of a sensitive assay to quantify GLUT4 mRNA in porcine adipose tissue will enable us to conduct studies to increase our understanding of the molecular mechanisms by which porcine somatotropin (pST) regulates GLUT4 gene expression.

This review summarizes the cross-sectional and training studies (acute and chronic) that have examined the relationship between exercise and plasma lipid and lipoproteins in women. Because women experience major fluctuations in reproductive hormones throughout the life cycle, the effects of the endogenous sex steroid status on the association between exercise and plasma lipoproteins also are addressed. In general, cross-sectional studies report a positive association between exercise and high density lipoprotein-cholesterol (HDL-C) in both pre- and postmenopausal women. Women on hormone replacement therapy who report exercising have higher HDL-C than sedentary women on hormone replacement therapy. Results from longitudinal training studies have been inconsistent because of experimental design, i.e., inadequate type, duration, and intensity of exercise intervention, lipid measurements made across the menstrual cycle, and studies carried out in women with high baseline HDL-C. Since lipids vary approximately 10-25% throughout the menstrual cycle, menstrual phase should be controlled when determining lipid changes after an exercise intervention. In approximately half of the intervention studies, an increase in HDL-C was demonstrated; the magnitude of the response that can be expected is approximately 10%. The responsiveness of pre- versus postmenopausal women to an exercise intervention is unknown. Studies are needed to clarify the interactive effects of exercise and sex hormones on plasma lipoproteins in women of all ages. This information will be useful in developing intervention programs to reduce the risk of coronary heart disease in women.

This article reviews the literature about the safety and benefits of two recombinantly derived proteins, bovine somatotropin (bST) and porcine somatotropin (pST), that likely will be used in animal agriculture in the future. When administered to dairy cows, bST increase milk production per cow approximately 15% to 20% and improves productive efficiency approximately 10%. Administration of pST to growing pigs reduces carcass fat content by as much as 70% to 80% and improves productive efficiency 15% to 35%. Because meat is a major source of total fat and saturated fatty acids in the diets of human beings, pST will allow consumers to include leaner, more nutrient-dense pork in their diets and still meet current dietary guidelines. Although these biotechnologies have not yet received regulatory approval from the Food and Drug Administration (FDA) for commercial use, information published by the FDA, the National Institutes of Health, the US Congress Office of Technology Assessment, and the American Academy of Pediatrics, as well as an extensive body of scientific evidence, indicate that these products are safe for the consumer. Nonetheless, it is important that consumers understand the benefits and safety of these biotechnologies. Dietitians can play an important role in providing information to consumers about the safety and benefits of bST and pST.

The present study was conducted to determine whether somatotropin (ST) binding sites are present in crude membrane preparations containing sarcolemma of pig skeletal muscle. Initial characterization experiments indicated that binding of bovine ST (bSTI was time- and tempera- ture-dependent and that binding was reversible. At 23"C, binding was maximized between 36 and 48 h, whereas at 4OC binding had not reached a maximum by 96 h. Somatotropin binding was stable between pH 5.5 and 8.5 and increased linearly between 100 and 600 pg of membrane protein. Addition of unlabeled bST decreased specific binding of [12511bST in a dose-dependent manner (EDs0: 1 to 1.6 ng/mL). The binding sites for bST were specific because porcine prolactin poorly inhibited bST binding. Scatchard analysis revealed the presence of a single class of binding sites (Ka: 9 to 15 x lO9M-I; Bmax: 5 to 6 fmol/mg of protein). In summary, the present report is the first to demonstrate that specific ST receptors are present in pig skeletal muscle. The role that ST plays in directly stimulating muscle growth and(or1 muscle synthesis of insulin-like growth factor I (IGF-I1 in pST-treated pigs as opposed to changes that occur as the result of an increase in plasma IGF-I concentration remains to be resolved. Key Words: Pigs, Somatotropin, Muscle, Receptors, Binding

International audience; A major objective of Animal Science is to develop feasible strategies to reduce lipid accretion during growth of meat animals. Historically, this objective has been sought because of the importance of reducing the quantity of nutrients used to produce body fat and the need to produce lower-fat meat. A fact of long-standing is that an animal’s feed efficiency decreases as the proportion of fat increases in body-weight gain. Thus, reducing fat deposition will improve feed efficiency (i.e. lower the feed:gain ratio) and, hence, increase productive efficiency (gaidfeed). A reduction in fat content of fresh meat also will benefit consumers who wish to decrease their intake of saturated fatty acids (SFA). A reduction in total fat intake to less than 30% of energy and SFA intake to less than 10% of energy is advised in the USA because of the positive relationship that exists between the quantity of SFA consumed and an elevation in plasma low-densitylipoprotein-cholesterol (LDL-C) which is a major risk factor for coronary heart disease (for review, see Kris-Etherton et al. 1988).During the past 10 years remarkable progress has been made in identifying feasible and effective strategies to reduce lipid accretion (Etherton & Kensinger, 1984; Boyd & Bauman, 1989; Etherton & Smith, 1991). The two strategies most likely to be used in production agriculture involve administering somtatotropin (ST) or p-adrenergic agonists to meat animals. In the present paper our current understanding of the mechanisms whereby ST and the P-agonists reduce adipose tissue growth will be reviewed.

The present study was undertaken to determine the number and size of growth hormone binding proteins present in pig adipose tissue, determine if there were differences in binding of pGH and bGH to adipose tissue membranes and establish the effects of pGH treatment on GH binding. Administration of pGH (0, 25, 50 or 100 micrograms pGH/kg BW/d) for 7 d did not affect binding of [125I]bGH to adipose tissue microsomes. Maximum binding of bGH was approximately 8-fold higher than that observed for pGH. Half-maximal inhibition of [125I]bGH binding was observed at 11 ng/ml of bGH. In contrast, a more than 10-fold greater concentration of pGH was required to half-maximally inhibit [125I]pGH binding. bGH and pGH both bound to the same GH binding proteins (Mr of 92,000, 73,000 and 53,000). The GH binding proteins appear to be produced by post-translational modification of a single GH receptor transcript rather than alternative splicing of a primary transcript since only one GH receptor mRNA transcript (4.2 kb) was detected on Northern analysis. Our findings indicate that: 1) bGH is the preferred ligand to use to study GH binding in pig adipose tissue membranes (or adipocytes); 2) exogenous pGH does not alter GH binding; and 3) only one GH receptor mRNA transcript is present in pig adipose tissue.