oxytocin and Hypertrophy

To understand the adaptation to lactation of obese rats, by studying the interplay among the gut hormone cholecystokinin (CCK), the adiposity hormone leptin and the affiliation hormone oxytocin in modulating body mass and fat storage.. Strain differences were examined between Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking expression of functional CCK-1 receptors and Long Evans Tokushima Otsuka (LETO) controls, tested as nulliparous dams, at the 7 and 15th lactation day, at weaning (lactation day 22) or 8 weeks postweaning.. We measured body mass, fat pads (brown, retroperitoneal and inguinal) and inguinal adipocytes. Plasma levels of leptin and oxytocin were determined.. Fat depots of LETO female rats were larger during lactation compared to the levels found in postweaning and nulliparous female rats. LETO female rats gained weight and accumulated fat during pregnancy and lactation, returning to their normal fat levels postweaning. In contrast, OLETF female rats presented lower body weight and fat depots during the lactation period than nulliparous dams, and regained the weight and fat postweaning. Plasma leptin and oxytocin were highly correlated and followed the same pattern. OLETF leptin levels were highly correlated with fat depot and inguinal cell surface. No significant correlation was found for LETO parameters.. Pregnancy and lactation are energy-consuming events, which naturally induce female rats to increase food intake and accumulate fat. When challenged by the demands of rapidly growing preobese OLETF pups, OLETF dams' fat stores are reduced to lean, LETO levels. During lactation, sensitivity of the oxytocinergic neurons descending from the paraventricular nuclei to the nucleus of the solitary tract to CCK is reduced. We theorized that this pathway is not available to OLETF female rats that lack functional CCK-1 receptors to mediate the signal. The current study contributes to the understanding of the female body's adaptation to lactation.

Topics: Adaptation, Physiological; Adipocytes; Adipose Tissue; Animals; Body Weight; Disease Models, Animal; Female; Hypertrophy; Lactation; Leptin; Mutation; Obesity; Oxytocin; Rats; Rats, Inbred OLETF; Receptors, Cholecystokinin; Weaning; Weight Gain

Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS.

Topics: Animals; Axons; Axotomy; Central Nervous System; Electron Transport Complex IV; Functional Laterality; Histocytochemistry; Hypertrophy; Hyponatremia; Hypothalamo-Hypophyseal System; In Situ Hybridization; Male; Microscopy, Electron; Nerve Regeneration; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Peptides; Pituitary Gland; Rats; Rats, Sprague-Dawley; RNA, Messenger; Supraoptic Nucleus; Time Factors; Vasopressins

Topics: Animals; Castration; Corpus Luteum; Female; Hypertrophy; Lactation; Ligation; Milk; Organ Size; Ovary; Oxytocin; Pregnancy; Rats; Spinal Cord; Sucking Behavior

Topics: Animals; Axons; Basement Membrane; Capillaries; Hypertrophy; Hypophysectomy; Hypothalamo-Hypophyseal System; Intercellular Junctions; Microscopy, Electron; Nerve Regeneration; Neurosecretory Systems; Oxytocin; Pituitary Gland, Posterior; Rats; Synaptic Vesicles; Vasopressins

Topics: Animals; Castration; Disease Models, Animal; Drug Antagonism; Female; Follicle Stimulating Hormone; Gonadotropins, Pituitary; Hypertrophy; Indoles; Melatonin; Mice; Ovarian Diseases; Ovulation; Oxytocin; Physiology, Comparative; Pineal Gland; Rodentia; Serotonin; Tissue Extracts; Vasopressins

Topics: Animals; Dogs; Estrogens; Female; Humans; Hypertrophy; Labor, Obstetric; Muscles; Oxytocin; Placenta; Pregnancy; Progesterone; Rabbits; Rats; Uterus