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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During cold-induced nonshivering thermogenesis, interscapular brown adipose tissue (BAT) lipoprotein lipase (LPL) activity and lipogenesis are elevated. Because of the many similarities between cold- and diet-induced thermogenesis, we examined the effect of ad libitum access to a 32% sucrose solution on caloric intake, adiposity, and BAT enzyme activities in male rats. Daily caloric intakes of sucrose-fed animals were elevated by 20%-25%, and 8 wk of sucrose feeding doubled carcass fat content. This sucrose-feeding induced obesity was associated with increases in circulating triglyceride and insulin levels as well as increased retroperitoneal white adipose tissue LPL activity. However, the increased carcass lipid content accounted for less than half of the excess calories ingested by the sucrose-fed rats. Sucrose feeding stimulated in vivo lipogenesis in BAT and elevated BAT fatty acid synthetase and acetyl-CoA carboxylase activities but not LPL activity. These findings suggest that overeating enhances endogenous lipogenesis but not uptake of circulating triglyceride in BAT. Thus, both cold- and diet-induced thermogenesis increase BAT lipogenesis, while only cold-induced thermogenesis is associated with elevated LPL activity in BAT.
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PMID:Effect of sucrose overfeeding on brown adipose tissue lipogenesis and lipoprotein lipase activity in rats. 682 91

The free-feeding, genetically obese rat is hyperphagic, hyperinsulinemic, and hypertriglyceridemic and has increased fat cell size and number compared to its lean littermate. These experiments demonstrate that, when fafa rats are prevented from expressing hyperphagia throughout life, the complete obese "syndrome" still develops. Furthermore, life-long food restriction does not prevent increased lipoprotein lipase in the fafa rat. The data support the concept that a peripheral metabolic adaptation, probably in lipid metabolism, results in preferential shunting of dietary substrate in the restricted obese rats to adipose tissue with concomitant decreases in other tissues.
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PMID:Development of obesity in Zucker obese (fafa) rat in absence of hyperphagia. 736 56

1. During the first two thirds of gestation, coinciding with a minimal accretion by the conceptus, the mother is in an anabolic state which is supported by her hyperphagia and the more efficient conservation of exogenous nutrients when she eats. During this phase maternal fat deposits are accumulated thanks to the enhancement in adipose tissue lipogenic and glycerologenic activity. In contrast, in the latter part of gestation, the rapid fetal growth is sustained by the intense transfer of nutrients from maternal circulation. 2. Glucose is quantitatively the most abundant of the several substrates that cross the placenta and despite increased maternal gluconeogenesis this transfer is responsible for the maternal tendency to hypoglycemia. This causes a switch to a net catabolic state which is especially evident in the net breakdown of fat depots. 3. Enhanced release of adipose tissue lipolytic products, free fatty acids (FFA) and glycerol, facilitates the liver synthesis of triglycerides and their later release into circulation associated to very low-density lipoprotein (VLDL). Glycerol is also used as an important gluconeogenic substrate and FFAs are broken down through beta-oxidation for ketone body synthesis. Flow through these pathways becomes increased when food is withheld and this actively contributes to the availability of fuels to the fetus which becomes partially preserved from maternal metabolic insult. Increased liver production of VLDL-triglycerides and decreased extrahepatic lipoprotein lipase contribute to exaggerated maternal hypertriglyceridemia which, besides being a floating metabolic reserve for emergency conditions such as starvation, constitutes an essential substrate for milk synthesis around parturition in preparation for lactation. 4. While the maternal anabolic tendencies found during the first two-thirds of gestation seem to be facilitated by hyperinsulinemia in the presence of a normal responsiveness to the hormone, it is proposed that most of the metabolic changes taking place during the last third of gestation seem to be caused by the insulin-resistant state which is consistently present at this stage, since its reversion caused by sustained exaggerated hyperinsulinemia also reverts several of these metabolic adaptations.
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PMID:Carbohydrate-lipid interactions during gestation and their control by insulin. 754 70

Chronic intracerebroventricular (icv) administration of neuropeptide-Y (NPY; 10 micrograms/day) was performed in normal female rats to investigate its hormonal and metabolic consequences. Intracerebroventricular NPY produced hyperphagia, increased basal insulinemia, as well as liver and adipose tissue lipogenic activity. It also increased basal morning corticosteronemia. When NPY-induced hyperphagia was prevented by pair-feeding, the icv NPY treatment resulted in the same increases in basal insulinemia and corticosteronemia, and liver and white adipose tissue lipogenesis was still higher than that in respective controls. Under the ad libitum and pair-feeding conditions, icv NPY stimulated glucose uptake as well as total lipoprotein lipase activity in white adipose tissue; it resulted in an increase total activity of hepatic and white adipose tissue acetyl coenzyme-A-carboxylase. As all hormonal and metabolic changes elicited by icv NPY remained present (at the same or to a lesser extent depending upon the parameter considered) when hyperphagia was prevented by pair-feeding, it was, thus, shown that icv NPY per se induces peripheral hormonal and metabolic alterations via efferent routes, which remain to be determined. The effects of icv NPY reported in this study are similar to the defects observed in the early phase of genetic obesity in rodents, the hypothalamus of which has increased NPY levels. NPY could, thus, be of relevance in the occurrence of genetically induced obesity.
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PMID:Chronic intracerebroventricular neuropeptide-Y administration to normal rats mimics hormonal and metabolic changes of obesity. 840 18

Obesity has a strong genetic component, which should be viewed as a predisposition only if certain environmental factors are present. Impaired regulation of both sides of the energy balance equation plays a role in the propensity to gain weight and develop obesity. Overeating may be induced in susceptible individuals by high dietary fat content, large portion sizes and low meal frequency. Increased metabolic efficiency in the form of a low resting metabolic rate has been identified in pre- and post-obese subjects, and the impact on total energy expenditure may be amplified by a low level of physical activity. A low thermic effect of food has been shown not to be a risk factor for weight gain, and post-obese subjects have a normal thermic effect of food. A genetically determined enhanced metabolic efficiency during overfeeding has been reported to contribute to fat gain. The heterogeneous nature of obesity indicates that different mechanisms, such as changes in the partitioning of fat (due to lipoprotein lipase activity, fat oxidative muscle enzymes) and carbohydrate, and an altered responsiveness of the sympathoadrenal system and thyroid hormones to a positive energy balance, seem to be involved.
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PMID:Obesity and metabolic efficiency. 901 80

During lactation in the rat, despite hyperphagia, there are no changes in either the plasma levels or the gene expression of leptin. Removal of the litter, however, results in an important increase in the circulating concentration of leptin. Administration of leptin to lactating rats resulted in no changes in the in vivo lipogenic rate and lipoprotein lipase (LPL) activity in either adipose tissue or mammary gland, although there was an increase in insulin levels as a consequence of leptin administration. Conversely, litter removal resulted in an important decrease of LPL activity and lipogenic rate in the mammary gland while an increase in these parameters took place in adipose tissue. It is concluded that leptin is not the signal responsible for the changes in lipid metabolism that take place both in adipose tissue and mammary gland following litter removal.
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PMID:Leptin administration to lactating rats is unable to induce changes in lipid metabolism in white adipose tissue or mammary gland. 1041 35

Our previous studies have shown that the dopaminergic D1 receptor agonist SKF38393 (SKF) plus the D2 receptor agonist bromocriptine (BC) act synergistically to reduce obesity in obese C57BL/6J (ob/ob) mice. The present study investigated the effects of this combination on dyslipidemia in ob/ob mice. Female ob/ob mice were treated daily with vehicle or SKF (20 mg/kg body weight [BW]) plus BC (16 mg/kg BW [BC/SKF]) for 14 days. The animals were then used for the characterization of plasma lipoprotein profiles, hepatic triacylglycerol synthesis and secretion, adipocyte lipolysis, adipose and muscle lipoprotein lipase (LPL) activity, and muscle triglyceride (TG) content. The treatment significantly reduced plasma glucose 54%, TG 41%, cholesterol 21%, phospholipid 20%, and free fatty acid (FFA) 36% (P < .01). Hepatic triacylglycerol synthesis was 55% lower in treated mice versus control mice (P < .01). The cell size of isolated adipocytes was significantly reduced (41%) by treatment. LPL activity was increased in soleus skeletal muscle (25%, P < .05) but was sharply reduced in adipose tissue (91%, P < .01) in treated versus control mice. The TG content of hindlimb muscle was about 49% lower in treated versus control mice (P < .05). The basal and isoproterenol-stimulated lipolytic rate was decreased (approximately 53%) in adipocytes from treated animals compared with the control (P < .01). In conclusion, BC/SKF normalized the hypertriglyceridemia likely via its simultaneous antilipogenic action in liver tissue and antilipolytic action in adipose tissue. Decreased plasma flux of FFA partially contributed to the reduced hepatic lipogenesis, plasma very-low-density lipoprotein (VLDL)-TG, and TG in skeletal muscle. The above-described effects of BC/SKF treatment are largely independent of its effect to normalize hyperphagia in ob/ob mice.
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PMID:Bromocriptine/SKF38393 treatment ameliorates dyslipidemia in ob/ob mice. 1045 70

During the first two-thirds of gestation, the mother is in an anabolic condition, increasing her fat depots thanks to both hyperphagia and enhanced lipogenesis. During the last third of gestation, the mother switches to a catabolic condition. Glucose is the most abundant nutrient crossing the placenta, which causes maternal hypoglycemia despite an increase in the gluconeogenetic activity. Adipose tissue lipolytic activity becomes enhanced, increasing plasma levels of FFA and glycerol that reach the liver; consequently there is an enhanced production of triglycerides that return to the circulation in the form of very low density lipoproteins (VLDL). Glycerol is also used as a preferential gluconeogenetic substrate, saving other more essential substrates, like amino acids, for the fetus. Under fasting conditions, fatty acids are converted into ketone bodies throughout the beta-oxidation pathway, and these compounds easily cross the placental barrier and are metabolized by the fetus. An enhanced liver production of VLDL-triglycerides together with a decrease in adipose tissue lipoprotein lipase (LPL) and an increase in plasma activity of cholesterol ester transfer protein causes both an intense increment in these lipoproteins and a proportional enrichment of triglycerides in both low and high density lipoproteins. Maternal triglycerides do not cross the placenta, but the presence of LPL and other lipases allows their hydrolysis, releasing fatty acids to the fetus. Under fasting conditions, the maternal liver uses circulating triglycerides as ketogenic substrates. Around parturition there is an induction of LPL activity in the mammary glands, driving circulating triglycerides to this organ for milk synthesis, allowing essential fatty acids derived from the mother's diet to become available to the suckling newborn.
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PMID:Metabolic adaptations in pregnancy and their implications for the availability of substrates to the fetus. 1080 38

During early pregnancy there is an increase in body fat accumulation, associated with both hyperphagia and increased lipogenesis. During late pregnancy there is an accelerated breakdown of fat depots, which plays a key role in fetal development. Besides using placental transferred fatty acids, the fetus benefits from two other products: glycerol and ketone bodies. Although glycerol crosses the placenta in small proportions, it is a preferential substrate for maternal gluconeogenesis, and maternal glucose is quantitatively the main substrate crossing the placenta. Enhanced ketogenesis under fasting conditions and the easy transfer of ketones to the fetus allow maternal ketone bodies to reach the fetus, where they can be used as fuels for oxidative metabolism as well as lipogenic substrates. Although maternal cholesterol is an important source of cholesterol for the fetus during early gestation, its importance becomes minimal during late pregnancy, owing to the high capacity of fetal tissues to synthesize cholesterol. Maternal hypertriglyceridemia is a characteristic feature during pregnancy and corresponds to an accumulation of triglycerides not only in very low-density lipoprotein but also in low- and high-density lipoprotein. Although triglycerides do not cross the placental barrier, the presence of lipoprotein receptors in the placenta, together with lipoprotein lipase, phospholipase A2, and intracellular lipase activities, allows the release to the fetus of polyunsaturated fatty acids transported as triglycerides in maternal plasma lipoproteins. Normal fetal development needs the availability of both essential fatty acids and long chain polyunsaturated fatty acids, and the nutritional status of the mother during gestation has been related to fetal growth. However, excessive intake of certain long chain fatty acids may cause both declines in arachidonic acid and enhanced lipid peroxidation, reducing antioxidant capacity.
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PMID:Lipid metabolism in pregnancy and its consequences in the fetus and newborn. 1258 1

To compare the effects of acute exposure to dietary fat to those of chronic exposure, Sprague-Dawley rats were given a high-fat diet (50% fat) or moderate-fat diet (25% fat) for 1 day, 2 h or 3 weeks. With measurements of various parameters, the high-fat diet for 21 days produced the expected changes of: (1) a significant increase in total caloric intake and dissected fat pad weights; (2) a rise in leptin and the metabolites, triglycerides (TG), non-esterified fatty acids and glucose; (3) an increase in muscle beta-hydroxyacyl-CoA dehydrogenase (HADH) and adipose lipoprotein lipase (aLPL) activity, along with a decrease in LPL activity in muscle (mLPL); and (4) elevated galanin (GAL) expression and peptide levels in the anterior region of the paraventricular nucleus (PVN), with no change in the arcuate nucleus. The acute 1-day or 2-h high-fat diet similarly increased circulating lipids, HADH activity and PVN GAL mRNA but stimulated rather than suppressed mLPL activity. These effects occurred in the absence of a change in total caloric intake, fat pad weights, and adipose-related measures, suggesting that they resulted more from the rise in dietary fat from 25% to 50% than from increased adiposity or hyperphagia. Moreover, PVN GAL mRNA in the different groups was consistently and positively correlated with the specific measures of TG levels and both HADH and mLPL activity, linking it to metabolic processes related to the transport and capacity for oxidation of TG in muscle, rather than adipose tissue.
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PMID:Acute high-fat diet paradigms link galanin to triglycerides and their transport and metabolism in muscle. 1514 53


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