Cigarette smoke during lactation in rat female progeny: Late effects on endocannabinoid and dopaminergic systems.

AIMS: Maternal smoking is considered a risk factor for childhood obesity. In a rat model of tobacco exposure during breastfeeding, we previously reported hyperphagia, overweight, increased visceral fat and hyperleptinemia in adult female offspring. Obesity and eating disorders are associated with impairment in the endocannabinoid (EC) and dopaminergic (DA) systems. Considering that women are prone to eating disorders, we hypothesize that adult female Wistar rats that were exposed to cigarette smoke (CS) during the suckling period would develop EC and DA systems deregulation, possibly explaining the eating disorder in this model. MATERIAL AND METHODS: To mimic maternal smoking, from postnatal day 3 to 21, dams and offspring were exposed to a smoking machine, 4×/day/1 h (CS group). Control animals were exposed to ambient air. Offspring were evaluated at 26 weeks of age. KEY FINDINGS: Concerning the EC system, the CS group had increased expression of diacylglycerol lipase (DAGL) in the lateral hypothalamus (LH) and decreased in the liver. In the visceral adipose tissue, the EC receptor (CB1r) was decreased. Regarding the DA system, the CS group showed higher dopamine transporter (DAT) protein expression in the prefrontal cortex (PFC) and lower DA receptor (D2r) in the arcuate nucleus (ARC). We also assessed the hypothalamic leptin signaling, which was shown to be unchanged. CS offspring showed decreased plasma 17ß-estradiol. SIGNIFICANCE: Neonatal CS exposure induces changes in some biomarkers of the EC and DA systems, which can partially explain the hyperphagia observed in female rats.

Impact of 1,25(OH) 2 D 3 on TG content in liver of rats with type 2 diabetes.

PURPOSE: To evaluate the effects of 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) on the content of triglyceride (TG), as well as on the gene and protein expressions of adiponectin receptor 2 (AdipoR2), p38 mitogen-activated protein kinase (P38MAPK), and lipoprotein lipase (LPL) in the liver of rats with type 2 diabetes mellitus (T2DM) so as to provide theoretical basis for exploring the mechanism by which 1,25(OH)2D3 regulates TG. METHODS: Wistar rats were divided into four groups (n=25), with different treatments and detected the gene and protein expressions of AdipoR2, p38MAPK, and LPL in the liver tissue by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Meanwhile, the content of TG in the liver tissue was detected by the Enzyme-linked immunosorbent assay. RESULTS: The expression of AdipoR2, p38MAPK, LPL gene and protein in the liver of VitD intervention group was significantly higher than that in T2DM group (P <0.05), while the TG content was significantly lower than that in T2DM group (P <0.05). CONCLUSION: 1,25(OH)2D3 can decrease the content of TG in the liver, and its mechanism may be achieved by upregulating the expressions of AdipoR2, p38MAPK, and LPL in the liver.

Impact of 1 25(OH) 2 D 3 on TG content in liver of rats with type 2 diabetes

Abstract Purpose: To evaluate the effects of 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) on the content of triglyceride (TG), as well as on the gene and protein expressions of adiponectin receptor 2 (AdipoR2), p38 mitogen-activated protein kinase (P38MAPK), and lipoprotein lipase (LPL) in the liver of rats with type 2 diabetes mellitus (T2DM) so as to provide theoretical basis for exploring the mechanism by which 1,25(OH)2D3 regulates TG. Methods: Wistar rats were divided into four groups (n=25), with different treatments and detected the gene and protein expressions of AdipoR2, p38MAPK, and LPL in the liver tissue by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Meanwhile, the content of TG in the liver tissue was detected by the Enzyme-linked immunosorbent assay. Results: The expression of AdipoR2, p38MAPK, LPL gene and protein in the liver of VitD intervention group was significantly higher than that in T2DM group (P <0.05), while the TG content was significantly lower than that in T2DM group (P <0.05). Conclusion: 1,25(OH)2D3 can decrease the content of TG in the liver, and its mechanism may be achieved by upregulating the expressions of AdipoR2, p38MAPK, and LPL in the liver.

Estrogen therapy attenuates adiposity markers in spontaneously hypertensive rats.

Ovarian hormones modulate the metabolism of adipose cells and present a protective effect against hypertension. The aim of this study was to compare the effect of estradiol on adiposity markers in spontaneously hypertensive rats. Ovariectomized spontaneously hypertensive rats treated with estradiol (5 µg/100 g/day), three weeks after ovariectomy, presented decreased blood pressure and insulin levels and increased hepatic glycogen content. Periuterine or mesenteric adipocytes from treated animals were smaller as compared to vehicle treated group, whereas no differences were observed in relation to the number of cells. Basal rates of glycerol release were higher only in periuterine adipocytes of treated rats. The increment of glycerol release over basal values in response to isoproterenol was 400% and 440%, 283% and 330% for vehicle and estradiol treated periuterine and mesenteric adipocytes, respectively. The estradiol treated group was more sensitive to insulin inhibition of isoproterenol-stimulated lipolysis than the control animals. The lipoprotein lipase activity decreased after treatment, only in periuterine adipose tissue. Estradiol administration increased basal and insulin-stimulated rates of glucose transport in adipocytes of both sites, although the values obtained by periuterine were higher than those observed for mesenteric adipocytes. Both adipose tissues from treated animals exhibited a decreased expression of the peroxisome proliferator-activated receptor-γ, but an increased expression of peroxisome proliferator-activated receptor-α in liver. These findings suggest that estrogen administration attenuates adiposity markers of spontaneously hypertensive rats as a result of the decreased expression levels of peroxisome proliferator-activated receptor-γ in adipose tissue and increased expression of peroxisome proliferator-activated receptor-α in liver.

Fatty acid synthesis and generation of glycerol-3-phosphate in brown adipose tissue from rats fed a cafeteria diet.

In vivo fatty acid synthesis and the pathways of glycerol-3-phosphate (G3P) production were investigated in brown adipose tissue (BAT) from rats fed a cafeteria diet for 3 weeks. In spite of BAT activation, the diet promoted an increase in the carcass fatty acid content. Plasma insulin levels were markedly increased in cafeteria diet-fed rats. Two insulin-sensitive processes, in vivo fatty acid synthesis and in vivo glucose uptake (which was used to evaluate G3P generation via glycolysis) were increased in BAT from rats fed the cafeteria diet. Direct glycerol phosphorylation, evaluated by glycerokinase (GyK) activity and incorporation of [U-14C]glycerol into triacylglycerol (TAG)-glycerol, was also markedly increased in BAT from these rats. In contrast, the cafeteria diet induced a marked reduction of BAT glyceroneogenesis, evaluated by phosphoenolpyruvate carboxykinase-C activity and incorporation of [1-14C]pyruvate into TAG-glycerol. BAT denervation resulted in an approximately 50% reduction of GyK activity, but did not significantly affect BAT in vivo fatty acid synthesis, in vivo glucose uptake, or glyceroneogenesis. The data suggest that the supply of G3P for BAT TAG synthesis can be adjusted independently from the sympathetic nervous system and solely by reciprocal changes in the generation of G3P via glycolysis and via glyceroneogenesis, with no participation of direct phosphorylation of glycerol by GyK.

Effect of variation of trans-fatty acid in lactating rats' diet on lipoprotein lipase activity in mammary gland, liver, and adipose tissue.

OBJECTIVE: Lactation is associated with an increase in lipoprotein lipase (LPL) activity in the mammary gland (MG) and a decrease in adipose tissue because lactation redirects circulating substrates to the MG for milk synthesis. We investigated the effects of different dietary contents of trans-fatty acid (TFA) on LPL activity in maternal tissues and fatty acid composition in milk. METHODS: Lactating rats were fed semisynthetic isocaloric diets containing 7% soy oil (control), 7% partially hydrogenated vegetable oil (7%-PHVO), 5% PHVO plus 2% soy oil (5%-PHVO), or 3.5% PHVO plus 3.5% soy oil (3.5%-PHVO). On lactation day 14, animals were decapitated and MG, liver, and parametrial adipose tissue were extracted to determine total lipid contents, percentages of TFA, and LPL activity. Milk lipid composition was examined by gas chromatographic analysis of the gastric content of 14-d-old suckling pups. RESULTS: Maternal consumption of TFA increased dietary TFA incorporation in MG and liver and decreased it in parametrial adipose tissue. Diets with higher trans concentrations (7%-PHVO) significantly increased lipid content in the MG, and all groups fed trans-based diets showed significant increases in LPL activity in the MG. Although LPL increased in the MG, milk of rats fed TFA-based diets had significant decreases in the percentage of essential fatty acids. CONCLUSIONS: TFA intake during lactation alters maternal lipid metabolism and the percentage of essential fatty acids in milk; therefore, it is important to alert the population to avoid excessive intake of TFAs during lactation.

[heparin and insulin treatment of acute pancreatitis caused by hypertriglyceridemia. Experience of 5 cases]. / Heparina e insulina en el tratamiento de la pancreatitis aguda por hipertrigliceridemia. Experiencia en 5 casos.

BACKGROUND: Hypertriglyceridemia over 1,000 mg/dl can provoke acute pancreatitis and its persistence can worsen the clinical outcome. On the contrary, a rapid decrease in triglyceride level is beneficial. Plasmapheresis has been performed in some patients to remove chylomicrons from the circulation, while heparin and/or insulin have been administered in some other cases to rapidly reduce blood triglycerides. Heparin and insulin stimulate lipoprotein-lipase activity and accelerate chylomicron degradation. AIM: To report five patients with acute pancreatitis treated with heparin and insulin. PATIENTS AND METHODS: Five patients (4 females and 1 male) seen in the last two years, who suffered acute pancreatitis induced by hypertriglyceridemia are reported. Initial blood triglyceride levels were above 1,000 mg/dl (range 1,590-8,690 mg/dl). Besides the usual treatment of acute pancreatitis, heparin and/or insulin were administered intravenously in continuous infusion. Heparin dose was guided by usual parameters of blood coagulation, and insulin dose, by serial determinations of blood glucose. Pancreatic necrosis was demonstrated in 4 patients. RESULTS: Serum triglyceride levels decreased to < 500 mg/dl within 3 days in all cases. No complication of treatment was observed and all patients survived. Early and late complications of pancreatitis occurred in one patient. CONCLUSION: Administration of heparin and/or insulin is an efficient alternative to reduce triglyceride levels in patients with acute pancreatitis and hypertriglyceridemia.