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Free fatty acids (FFAs) are rapidly mobilized by ACTH and have been shown to be potent endogenous modulators of steroid-protein interactions. We increased FFA in lagomorphs by ACTH and then separated the transient increase in glucocorticoid binding capacity of plasma into that accounted for by changes in binding to albumin and to corticosteroid-binding globulin (CBG). Sequential injections of dexamethasone and ACTH into both snowshoe hares and laboratory rabbits resulted in the rapid mobilization of FFA only after the ACTH injection. The maximum corticosteroid binding capacity increase paralleled that of the FFA increase in both species. In rabbits, CBG levels remained constant over the duration of the experiment. Corticosterone binding by rabbit albumin increased in a dose-dependent fashion in response to increases in FFA (oleic and linoleic acid) concentrations. Finally, by stimulating FFA release in snowshoe hares with ACTH and separating the increase in corticosteroid binding capacity through selective denaturing of CBG by heat, we determined that the increase in plasma binding capacity was a response to changes in binding by albumin, not CBG. Thus FFA released in response to stressors in lagomorphs may effect short-term increases in steroid binding.
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The pyruvate dehydrogenase kinases (PDK1-4) regulate glucose oxidation through inhibitory phosphorylation of the pyruvate dehydrogenase complex (PDC). Immunoblot analysis with antibodies raised against recombinant PDK isoforms demonstrated changes in PDK isoform expression in response to experimental hyperthyroidism (100 microg/100 g body weight; 3 days) that was selective for fast-twitch vs slow-twitch skeletal muscle in that PDK2 expression was increased in the fast-twitch skeletal muscle (the anterior tibialis) (by 1. 6-fold; P<0.05) but not in the slow-twitch muscle (the soleus). PDK4 protein expression was increased by experimental hyperthyroidism in both muscle types, there being a greater response in the anterior tibialis (4.2-fold increase; P<0.05) than in the soleus (3.2-fold increase; P<0.05). The hyperthyroidism-associated up-regulation of PDK4 expression was observed in conjunction with suppression of skeletal-muscle PDC activity, but not suppression of glucose uptake/phosphorylation, as measured in vivo in conscious unrestrained rats (using the 2-[(3)H]deoxyglucose technique). We propose that increased PDK isoform expression contributes to the pathology of hyperthyroidism and to PDC inactivation by facilitating the operation of the glucose --> lactate --> glucose (Cori) and glucose --> alanine --> glucose cycles. We also propose that enhanced relative expression of the pyruvate-insensitive PDK isoform (PDK4) in skeletal muscle in hyperthyroidism uncouples glycolytic flux from pyruvate oxidation, sparing pyruvate for non-oxidative entry into the tricarboxylic acid (TCA) cycle, and thereby supporting entry of acetyl-CoA (derived from fatty acid oxidation) into the TCA cycle.
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The ability of GH to decrease fatness and insulin-regulated events such as lipogenic enzyme activities is well known in pigs. Nevertheless, the precise mechanism underlying these actions has not been elucidated yet. Expression of the transcription factor sterol regulatory element binding protein (SREBP)-1 has been reported as a key mediator of insulin action in rat hepatocytes and adipose cell lines. The present study aimed to determine whether the regulation of lipogenesis by GH and/or insulin in porcine adipocytes also involved SREBP-1. Isolated adipocytes, obtained from perirenal or s.c. adipose tissue samples of female pigs (51+/-0.4 kg; n=17), were cultured in serum-free medium in the absence or presence of these hormones for up to 4 days. Glucose incorporation and fatty acid synthase activity were increased by insulin in a dose-dependent manner in adipocytes of both sites. The increase was maximal at 1.7 and 17 nM in s.c. and perirenal adipocytes respectively, suggesting inter-depot differences in the regulation of lipogenesis by insulin. These insulin-stimulated events were decreased by GH (1 nM). No change in SREBP-1 mRNA levels was observed in response to GH and/or insulin. Taken together, these data indicate that the regulation of lipogenesis by insulin and GH appears to not involve changes in SREBP-1 mRNA levels in porcine adipocytes.
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SUMMARY
The plasma sugar, free fatty acids (FFA), 11-hydroxycorticosteroids (11-OHCS) and growth hormone (GH) response to insulin-induced hypoglycaemia, have been studied in 19 patients with primary myxoedema and 13 normal subjects. Nine of the myxoedematous patients were restudied after treatment. The plasma 11-OHCS response to lysine vasopressin (LVP) was studied in the myxoedematous subjects and again in eight of them after treatment.
In myxoedema the plasma sugar falls to a lesser extent and more slowly in response to insulin than normal and takes longer to recover. The fall in plasma FFA is not different from normal, but recovery of plasma FFA is delayed. The responses to insulin-induced hypoglycaemia of plasma GH and 11-OHCS may be smaller than normal in myxoedema and tend to improve on treatment. Altered GH and 11-OHCS responses to insulin-induced hypoglycaemia in myxoedema are not necessarily due to pituitary or hypothalamic dysfunction. No difference was found in the response of plasma 11-OHCS to LVP before and after treatment. Pituitary function cannot be fully assessed in the presence of hypothyroidism.
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Recording electrodes were implanted in contact with the dura mater overlying the parietal cortex of six female goats, four of which were lactating. After recovery from surgery and complete familiarization with the housing conditions, the personnel and the recording technique, each goat was observed continuously for 24 h with simultaneous recording of the cortical electroencephalogram (EEG). Remote blood sampling was carried out every 30 min without disturbing the animal. Apart from the release of growth hormone (GH) associated with morning milking in two of the goats, there was no consistent relationship between the apparently spontaneous, episodic release of GH and behaviour, stages of sleep, cortical EEG, air temperature, time of day or night, obvious environmental stimuli which arose from the normal husbandry routine, or the levels of prolactin, insulin, glucose or free fatty acids in the blood. There was also no relationship between the release of prolactin and the stages of sleep.
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experimental arthritis. Eicosapentaenoic acid (EPA) is an n-3 polyunsaturated fatty acid that is essential for normal growth and is present in large amounts in fish oil. It is well known that EPA has an anti-inflammatory effect decreasing proinflammatory
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order to meet the systemic energy demands during a fast, hormonal signals stimulate adipose tissue to release non-esterified fatty acids (NEFA) into circulation at a rate which exceeds clearance by non-hepatic tissues ( Patel et al. 2002 , Djurhuus
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The increases in liver and blood lipid contents which occur at the onset of lay in the fowl can be simulated in the immature pullet by oestrogen administration (Lorenz, 1954). The liver is the major site of lipogenesis (Goodridge, 1968) and also of oestrogen-induced lipaemia (Ranney & Chaikoff, 1951). Androgens and progestagens are also involved in the physiological changes encountered at point-of-lay (see Balnave & Pearce, 1974) but neither affects the total blood or liver lipid content. Balnave (1968, 1969) suggested that testosterone and progesterone can influence hepatic lipid metabolism and gonadal hormones other than oestrogens can affect hepatic lipogenic enzyme activities (Pearce & Balnave, 1973; Balnave & Pearce, 1974). The present experiments investigated the hypothesis (Balnave, 1968) that gonadal hormones may also affect lipid degradation.
Four-week-old pullets, given food and water ad libitum, received i.m. injections, in 0·2 ml corn oil, of either 2 mg oestradiol dipropionate, 2 mg
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