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Eighteen Chianina crossbred steers were used to examine the interrelationship between hormonal status and empty body protein (EBPRT) and fat (EBFAT) accretion during an 88-d controlled realimentation (REAL; DMI was adjusted weekly on an individual BW basis) period. Body composition was determined by monitoring endogenous whole-body 40|K~. At the end of restriction (REST) and on d 31 and 59 of REAL blood samples were taken and analyzed for concentrations of growth hormone (GH), IGF-I, IGF-II, insulin (INS), thyroxine (|T.sub.4~), triiodothyronine (|T.sub.3~), reverse triiodothyronine (r|T.sub.3~), nonesterified fatty acids (NEFA), glucose, and urea nitrogen. Depositions of EBPRT and EBFAT were decreased (P |is less than~ .001) in REST (92 d) animals compared with nonrestricted (NR) controls. During REST, plasma levels of glucose, IGF-I, INS, |T.sub.4~, |T.sub.3~, and r|T.sub.3~ were decreased (P |is less than~ .05); plasma urea nitrogen (PUN), NEFA, and GH levels were increased (P |is less than~ .05), and IGF-II concentrations were similar between REST and NR steers. A transient compensatory response in BW gain and protein deposition occurred in repleted steers between d 35 and 62 of REAL. During this period, PUN levels markedly declined (P |is less than~ .01) in REAL steers and glucose concentration increased (P |is less than~ .01) to levels similar to those in NR controls. This response prevailed even though apparent digestible nutrients were decreased in repleted animals. During energy repletion, plasma levels of |T.sub.4~, |T.sub.3~, r|T.sub.3~, IGF-I, and INS were positively, and of GH was negatively, correlated with EBPRT and EBFAT gain in repleted animals. Unlike IGF-I, IGF-II was not correlated with compensatory body growth. These results suggest that compensating steers are more metabolically efficient; rapid body tissue gain occurs during a period of reduced nutrient digestibility. Additionally, plasma levels of IGF-I, GH, INS, and thyroid hormones, but not of IGF-II, are markedly affected by alteration of energy intake and are highly correlated with empty body gain and protein deposition in compensating late-maturing steers.

The effect of anabolic steroids on skeletal muscle protein metabolism in cattle was investigated. Circulating concentrations of growth hormone, insulin and cortisol as well as skeletal muscle protein breakdown were assessed in steers before and after implantation with estrogen (E), trenbolone acetate (TBA), or E + TBA. The results showed that estrogen implantation increased muscle protein deposition in steers, and this effect was enhanced when estrogen was combined with TBA. Furthermore, increased muscle protein was not due to a decrease in muscle protein degradation.

Background Although individuals with diabetes mellitus frequently have dyslipidaemias and high blood pressure, much of the increased risk for coronary heart disease is not explained by these and other classical risk factors. Thus, other less widely recognized risk factors, including increased susceptibility of low-density lipoprotein (LDL) to oxidation, might enhance vascular dysfunction and atherogenesis in diabetes.Aims We compared both the rate and extent of LDL oxidation ex vivo between 78 poorly controlled individuals with type 1 diabetes and 78 age- and sex-matched non-diabetic controls. We then initiated intensive insulin therapy for 3 months to determine the impact of improved glucose control on LDL composition and oxidation.Results Diabetic and non-diabetic individuals did not have significantly different body weights, dietary intake, blood pressure, renal function or plasma lipid levels. LDL composition was also similar in both groups. In contrast, vitamin E content in LDL was significantly lower in diabetic patients. Measures of LDL lipid oxidation, including conjugated diene, lipid peroxide and thiobarbituric acid reactive substances formation, as well as measures of LDL protein modification, were significantly greater in diabetic patients. Levels of hyperglycaemia correlated strongly with each measure of LDL lipid oxidation (r ranges from 0·60–0·81,P <0·05 for each correlation). After improved glucose control (average reduction in % HbAlcof 5·5 units) all measures of LDL oxidation improved dramatically and approached values for non-diabetics. Absolute values of LDL oxidation increased among all categories of age in both diabetic and control individuals, and this relationship persisted even after adjustment for differences in glucose concentrations.Conclusions We demonstrate that hyperglycaemia has a potent but reversible effect on LDL oxidation and that age may independently enhance LDL susceptibility to oxidation. These pathophysiological effects may play an important role in determining vascular complications and atherogenesis in poorly controlled type 1 diabetic patients. [ABSTRACT FROM PUBLISHER]