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School of Biomedical Sciences, Centre for Clinical Research, Endocrine Research Unit, Institute for Molecular Bioscience, University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia
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a pivotal physiological adaptation to promote insulin-driven lipogenesis, thereby preventing hyperlipidemia ( Cornford et al . 2012 ). Based on our observations, we propose an extension of the findings by Cornford et al . (2012) and anticipate
IRGS, Biogem, Ariano Irpino, Avellino, Italy
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IEOS-CNR, Naples, Italy
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Molecular Medicine and Medical Biotechnologies, University of Naples ‘Federico II’, Naples, Italy
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IRGS, Biogem, Ariano Irpino, Avellino, Italy
IEOS-CNR, Naples, Italy
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to be reduced ( Fig. 6D ). We verified the expression of genes involved in ‘ de novo lipogenesis’. acc mRNA was increased in all conditions in females, although this was not statistically significant in (CPF 300 nM) and (ETU + CPF 300 nM) females
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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
Progesterone in vitro decreases the rates of glucose uptake and of acetate uptake and oxidation, of lipogenesis from acetate and of oxygen consumption, and reduces the intracellular concentrations of ATP and citrate in slices of luteinized rat ovary incubated in a bicarbonate-buffered medium. The effect on glucose uptake was shown to be due to inhibition by progesterone of the membrane transport of glucose. In view of the steroid concentrations used to elicit these effects in vitro and the known actions of steroids such as progesterone on biological membranes, these observations are thought to be due to non-physiological lytic effects.
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The plasma insulin response to glucose and arginine was increased in intact female rats implanted with progesterone. This change was not mediated by increased energy intake since the insulin response to glucose was similarly enhanced in progesterone-treated rats pair-fed with controls. In contrast, similar levels of pancreatic glucagon were observed in the plasma of both control and experimental rats during arginine stimulation. Thus the molar ratio of insulin to glucagon may be increased in the plasma of progesterone-treated rats following a mixed meal. This change may represent a physiological adaption to a demonstrable resistance to the peripheral actions of insulin in non-adipose soft tissue. The hyperglycaemic and lipolytic actions of exogenous glucagon were also impaired in progesterone-treated rats. It is suggested that an increase in the molar ratio of insulin to glucagon will favour hepatic lipogenesis and the peripheral deposition of fat.
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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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Female rats implanted with progesterone gained weight more rapidly than control animals and had an increased proportion of total body fat. Restriction of food intake to control levels demonstrated that the weight change was not dependent on increased energy intake. Serum concentrations of cholesterol, phospholipid and non-esterified fatty acid were raised in hormone-treated rats but triglyceride levels were normal. Endogenous production of triglyceride was also unchanged. Total postheparin lipoprotein lipase activity was increased in the plasma of progesterone-treated rats largely due to increased release of the extrahepatic protamine sulphate-labile fraction. The basal rate of lipogenesis was also increased in adipocytes isolated from hormone-treated rats as was the insulin-stimulated rate of oxidation of [1-14C]glucose. Basal and adrenaline-stimulated rates of fat cell lipolysis were, however, unchanged by treatment with progesterone.
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ABSTRACT
Lipogenesis and blood glucose concentrations were determined at 4-hourly intervals in control and insulin-treated golden hamsters maintained on 14-h daily photoperiods (08·00–22·00 h). Lipogenesis was studied by measuring the incorporation of label into liver and fat pad lipids in animals killed 30 min after i.p. [3H]acetate injection and 2 h after insulin or saline (control) injections. Circadian rhythms of lipogenesis and plasma glucose concentration were present in both control and insulin-treated hamsters. In control animals most lipogenic activity occurred during the dark period and early during the daily photoperiod (14 h light: 10 h darkness). There were dramatic differences in the lipogenic (fat pad) and hypoglycaemic responses to insulin which varied as a function of the time of day at which insulin was injected. Insulin stimulated fivefold increases in lipid deposition (fat pad incorporation) when injected late during the dark period but had little or no effect 4–8 h after the onset of light. Daily injections for 8 days also produced variable cumulative effects on body fat stores as a function of the time of day. Insulin injected late during the dark period stimulated a 40% increase in abdominal fat weight over controls, whereas insulin injected at 4 and 12 h after the onset of light had no effect on abdominal fat weight. Insulin decreased plasma glucose concentrations markedly at 8 and 20–24 h after the onset of light but had no apparent hypoglycaemic activity (120 min after its injection) at 4 h after the onset of light. These response rhythms coupled with rhythms of insulin secretion provide a basis for temporal synergisms which could produce a spectrum of physiological conditions as a function of the phase relations between the rhythms.
J. Endocr. (1984) 103, 141–146
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Abstract
Transgenic mice were made by introducing extra copies of the mouse insulin-like growth factor-II (IGF-II) gene driven by the bovine keratin 10 promoter (BKVI). The adult plasma IGF-II levels were elevated at least three times in one line. In this line, there was a lower lipid content of both brown and white adipose depots at 2–4 months of age, and 40% less fat in the carcass at 7–9 months. The low lipid phenotype was not detected in the carcass at 2 weeks after birth. The lean characteristic was attributed to circulating IGF-II because the transgene was not expressed in fat. At 2–4 months of age, the transgenes oxidized more oral lipid, and less of this lipid was incorporated into the whole body and the epididymal fat. In contrast, the interscapular brown adipose tissue maintained lipid incorporation and lipoprotein lipase activity despite its reduced size. The altered activity of the brown adipose tissue may account for the gradual onset and persistence of the lean feature of the transgenic mice. There were no substantial changes in lipogenesis which could account for the low fat content. The plasma levels of IGF-I, insulin, glycerol, non-esterified fatty acids, triacylglycerols and glucose were not greatly changed and the pituitary GH content was within the normal range.
Journal of Endocrinology (1994) 143, 433–439
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ABSTRACT
Milk yield declined significantly between days 22 and 28 of lactation in rats, when lactation was extended by frequent replacement of older litters with younger ones. Corticosterone implants but not cortisol injections or implants prevented this decline. Cortisol, however, appeared to inhibit milk ejection since the mammary glands became engorged with milk and milk yield was improved dramatically by oxytocin injections. In both cases corticosteroid concentrations increased approximately threefold above basal concentrations.
Both corticosteroids increased total mammary gland RNA content and lipoprotein lipase (LPL) activity of the mammary gland but were without effect on insulin binding. They also decreased LPL activity, lipogenesis and the number of insulin receptors on adipose tissue.
Serum prolactin and insulin concentrations were unaffected by any of the treatments.
The results suggest that corticosteroids (1) inhibit milk ejection under certain conditions, (2) may be circulating in lower concentrations, which thereby limit milk production, during prolonged lactation and (3) may improve milk yield during extended lactation in part by suppressing anabolic activity in adipose tissue.
J. Endocr. (1984) 103, 213–218
