Early weaning alters the thermogenic capacity of brown adipose tissue in adult male and female rats.

PURPOSE: Early weaning (EW) is a risk factor for obesity development. Brown adipose tissue (BAT) hypofunction is related to obesity onset. Here, we evaluated whether sympathetic nervous system (SNS) activity in BAT and the thermogenic function of BAT are decreased in adulthood in obese rats from two EW models. METHODS: At the time of birth, lactating Wistar rats and their pups (three males and three females) were separated into three groups: the control group, in which pups consumed milk throughout lactation; the non-pharmacological EW (NPEW) group, in which suckling was interrupted with a bandage during the last 3 days of lactation; and the pharmacological EW (PEW) group, in which dams were treated with bromocriptine (0.5 mg/twice a day) 3 days before weaning. The offspring were sacrificed on PN180. RESULTS: Adult male rats from both EW models exhibited lower BAT SNS activity. Female rats from the PEW group showed a decrease in BAT SNS activity. The protein levels of UCP1 were lower in the NPEW males, while PGC1α levels were lower in both PEW and NPEW males. Both groups of EW females showed reductions in the levels of ß3-AR, TRß1, and PGC1α. The UCP1 protein level was reduced only in the NPEW females. The EW groups of both sexes had lower AMPK protein levels in BAT. In the hypothalamus, only the PEW females showed an increase in AMPK protein levels. In both groups of EW males, adrenal catecholamine was increased and tyrosine hydroxylase was decreased, while in EW females, adrenal catecholamine was decreased. CONCLUSIONS: Early weaning alters the thermogenic capacity of BAT, which partially contributes to obesity in adulthood, and there are sex-related differences in these alterations.

Solid-state sensors based on Eu3+-containing supramolecular polymers with luminescence colour switching capability.

Polymers that exhibit changes of their luminescence colour in response to external stimuli are attractive candidates for sensing systems. We herein report the preparation of europium-based metallosupramolecular polymers, which can be processed into films and coatings that display readily detectable luminescence colour changes in response to various types of analytes.

Neonatal tobacco smoke reduces thermogenesis capacity in brown adipose tissue in adult rats.

Maternal smoking is a risk factor for progeny obesity. We have previously shown, in a rat model of neonatal tobacco smoke exposure, a mild increase in food intake and a considerable increase in visceral adiposity in the adult offspring. Males also had secondary hyperthyroidism, while females had only higher T4. Since brown adipose tissue (BAT) hypofunction is related to obesity, here we tested the hypothesis that higher levels of thyroid hormones are not functional in BAT, suggesting a lower metabolic rate. We evaluated autonomic nerve activity in BAT and its function in adult rats that were exposed to tobacco smoke during lactation. At birth, litters were adjusted to 3 male and 3 female pups/litter. From postnatal day (PND) 3 to 21, Wistar lactating rats and their pups were divided into SE group, smoke-exposed in a cigarette smoking machine (4 times/day) and C group, exposed to filtered air. Offspring were sacrificed at PND180. Adult SE rats of both genders had lower interscapular BAT autonomic nervous system activity, with higher BAT mass but no change in morphology. BAT UCP1 and CPT1a protein levels were decreased in the SE groups of both genders. Male SE rats had lower ß3-AR, TRα1, and TRß1 expression while females showed lower PGC1α expression. BAT Dio2 mRNA and hypothalamic POMC and MC4R levels were similar between groups. Hypothalamic pAMPK level was higher in SE males and lower in SE females. Thus, neonatal cigarette smoke exposure induces lower BAT thermogenic capacity, which can be obesogenic at adulthood.

Neonatal tobacco smoke reduces thermogenesis capacity in brown adipose tissue in adult rats

Maternal smoking is a risk factor for progeny obesity. We have previously shown, in a rat model of neonatal tobacco smoke exposure, a mild increase in food intake and a considerable increase in visceral adiposity in the adult offspring. Males also had secondary hyperthyroidism, while females had only higher T4. Since brown adipose tissue (BAT) hypofunction is related to obesity, here we tested the hypothesis that higher levels of thyroid hormones are not functional in BAT, suggesting a lower metabolic rate. We evaluated autonomic nerve activity in BAT and its function in adult rats that were exposed to tobacco smoke during lactation. At birth, litters were adjusted to 3 male and 3 female pups/litter. From postnatal day (PND) 3 to 21, Wistar lactating rats and their pups were divided into SE group, smoke-exposed in a cigarette smoking machine (4 times/day) and C group, exposed to filtered air. Offspring were sacrificed at PND180. Adult SE rats of both genders had lower interscapular BAT autonomic nervous system activity, with higher BAT mass but no change in morphology. BAT UCP1 and CPT1a protein levels were decreased in the SE groups of both genders. Male SE rats had lower β3-AR, TRα1, and TRβ1 expression while females showed lower PGC1α expression. BAT Dio2 mRNA and hypothalamic POMC and MC4R levels were similar between groups. Hypothalamic pAMPK level was higher in SE males and lower in SE females. Thus, neonatal cigarette smoke exposure induces lower BAT thermogenic capacity, which can be obesogenic at adulthood.

Maternal high-fat diet induces obesity and adrenal and thyroid dysfunction in male rat offspring at weaning.

Maternal nutritional status affects the future development of offspring. Both undernutrition and overnutrition in critical periods of life (gestation or lactation) may cause several hormonal changes in the pups and programme obesity in the adult offspring. We have shown that hyperleptinaemia during lactation results in central leptin resistance, higher adrenal catecholamine secretion, hyperthyroidism, and higher blood pressure and heart rate in the adult rats. Here, we evaluated the effect of a maternal isocaloric high-fat diet on breast milk composition and its impact on leptinaemia, energy metabolism, and adrenal and thyroid function of the offspring at weaning. We hypothesised that the altered source of fat in the maternal diet even under normal calorie intake would disturb the metabolism of the offspring. Female Wistar rats were fed a normal (9% fat; C group) or high-fat diet (29% fat as lard; HF group) for 8 weeks before mating and during pregnancy and lactation. HF mothers presented increased total body fat content after 8 weeks (+27%, P < 0.05) and a similar fat content at the end of lactation. In consequence, the breast milk from the HF group had higher concentration of protein (+18%, P < 0.05), cholesterol (+52%, P < 0.05) and triglycerides (+86%, P < 0.05). At weaning, HF offspring had increased body weight (+53%, P < 0.05) and adiposity (2 fold, P < 0.05), which was associated with lower ß3-adrenoreceptor content in adipose tissue (-40%, P < 0.05). The offspring also presented hyperglycaemia (+30%, P < 0.05) and hyperleptinaemia (+62%, P < 0.05). In the leptin signalling pathway in the hypothalamus, we found lower p-STAT3/STAT3 (-40%, P < 0.05) and SOCS3 (-55%, P < 0.05) content in the arcuate nucleus, suggesting leptin resistance. HF offspring also had higher adrenal catecholamine content (+17%, P < 0.05), liver glycogen content (+50%, P < 0.05) and hyperactivity of the thyroid axis at weaning. Our results suggest that a high fat diet increases maternal body fat and this additional energy is transferred to the offspring during lactation, since at weaning the dams had normal fat and the pups were obese. The higher fat and protein concentrations in the breast milk seemed to induce early overnutrition in the HF offspring. In addition to storing energy as fat, the HF offspring had a larger reserve of glycogen and hyperglycaemia that may have resulted from increased gluconeogenesis. Hyperleptinaemia may stimulate both adrenal medullary and thyroid function, which may contribute to the development of cardiovascular diseases. These early changes induced by the maternal high-fat diet may contribute to development of metabolic syndrome.

[The relationship between lipid peroxidation and platelet aggregation in atherosclerotic patients]. / Relación entre la peroxidación lipídica y la agregación plaquetaria en pacientes ateroscleróticos.

We studied 58 patients with arterial esteno-occlusive disease, 32 diabetics and 26 nondiabetics. Some parameters of lipid metabolism and platelet function were evaluated. We show the correlations founded among these parameters and we offer a possible explanation which support this behaviour.