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Dans cet article à vocation théorique, les auteurs discutent des possibilités d’une psychanalyse post-œdipienne et d’un au-delà de la notion de différence des sexes.

Background/Objectives:: Adiponectin has a pivotal role in linking fat distribution with cardiometabolic disorders. We investigated the associations of long-term changes in circulating adiponectin with body composition and fat distribution at different abdominal depots in response to weight-loss dietary interventions, as well as the modification effect of sex. Subjects/Methods:: In the 2-year Preventing Overweight Using Novel Dietary Strategies (POUNDS Lost) Trial, 811 overweight or obese adults were randomly assigned to one of four diets varying in macronutrient intakes. Circulating concentrations of adiponectin were repeatedly measured at baseline, 6 months and 2 years. Body composition and fat distribution were repeatedly measured by dual-energy X-ray absorptiometry scan (n=424) and computed tomography (n=195). Results:: Over the 2-year intervention, after adjustment for age, sex, ethnicity, follow-up time, diet group, baseline body mass index and baseline level of respective outcome trait, increase of adiponectin was significantly associated with reduction of total fat mass (FM), total fat-free mass (FFM), whole body total percentage of fat mass (FM%), percentage of trunk fat (TF%), total adipose tissue (TAT), and adipose tissue mass at different depots including visceral (VAT), deep subcutaneous (DSAT) and superficial subcutaneous (SSAT; P<0.03 for each). The relations with FM, FM%, TF%, VAT and DSAT were significantly modified by sex (Pfor interaction=0.02, 0.005 and <0.001, 0.002, 0.03, respectively) with greater reductions associated with increase of adiponectin in men than in women. Conclusions:: Long-term changes in circulating adiponectin were differentially associated with improvement of body composition and abdominal fat distribution in men and women.

Objective:: Weight-loss intervention through diet modification has been widely used to improve obesity-related hyperglycemia; however, little is known about whether genetic variation modifies the intervention effect. We examined the interaction between weight-loss diets and genetic variation of fasting glucose on changes in glycemic traits in a dietary intervention trial. Research design and methods:: The Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial is a randomized, controlled 2-year weight-loss trial. We assessed overall genetic variation of fasting glucose by calculating a genetic risk score (GRS) based on 14 fasting glucose-associated single nucleotide polymorphisms, and examined the progression in fasting glucose and insulin levels, and insulin resistance and insulin sensitivity in 733 adults from this trial. Results:: The GRS was associated with 6-month changes in fasting glucose (P<0.001), fasting insulin (P=0.042), homeostasis model assessment of insulin resistance (HOMA-IR, P=0.009) and insulin sensitivity (HOMA-S, P=0.043). We observed significant interaction between the GRS and dietary fat on 6-month changes in fasting glucose, HOMA-IR and HOMA-S after multivariable adjustment (P-interaction=0.007, 0.045 and 0.028, respectively). After further adjustment for weight loss, the interaction remained significant on change in fasting glucose (P=0.015). In the high-fat diet group, participants in the highest GRS tertile showed increased fasting glucose, whereas participants in the lowest tertile showed decreased fasting glucose (P-trend <0.001); in contrast, the genetic association was not significant in the low-fat diet group (P-trend=0.087). Conclusions:: Our data suggest that participants with a higher genetic risk may benefit more by eating a low-fat diet to improve glucose metabolism.

Few well-controlled trials have evaluated the effects that macronutrient composition has on changes in food cravings during weight loss treatment. The present study, which was part of the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial, investigated whether the fat and protein content of four different diets affected changes in specific food cravings in overweight and obese adults. A sample of 811 adults were recruited across two clinical sites, and each participant was randomly assigned to one of four macronutrient prescriptions: 1) low fat (20% of energy), average protein (15% of energy); 2) moderate fat (40%), average protein (15%); 3) low fat (20%), high protein (25%); 4) moderate fat (40%), high protein (25%). With few exceptions, the type of diet that participants were assigned did not differentially affect changes in specific food cravings. Participants assigned to the high-fat diets, however, had reduced cravings for carbohydrates at month 12 (p<0.05) and fruits and vegetables at month 24. Also, participants assigned to high-protein diets had increased cravings for sweets at month 6 and month 12 (ps<0.05). Participants in all four dietary conditions reported significant reductions in food cravings for specific types of foods (i.e., high fat foods, fast food fats, sweets, and carbohydrates/starches; all ps<0.05). Cravings for fruits and vegetables, however, were increased at month 24 (p<0.05). Calorically restricted diets (regardless of their macronutrient composition) yielded significant reductions in cravings for fats, sweets, and starches whereas cravings for fruits and vegetables were increased.

The effects of adrenalectomy on the obese mouse were compared using animals which were weight-matched by controlled food intake. Adrenalectomy reduces weight gain of obese (ob/ob) mice. The reduced insulin and glucose after adrenalectomy are largely the result of reduced food intake. Changes in thyroid function are related to both the changes in food intake and to adrenalectomy itself.

The expression of specific calcium binding proteins is being used increasingly as a potential neuroanatomical marker for neurons with similar functions. In this study, the distribution of calbindin D28k in the superior colliculus (SC) of adult hamsters was examined by light and electron microscopy. Calbindin immunoreactivity was prominent in specific regions and laminae of the SC throughout its rostrocaudal extent, and was found to label horizontal, vertical and stellate cell types. In addition, calbindin label highlighted “bridges” of neuronal processes in the intermediate layers. The most frequent calbindin-immunoreactive profiles seen in the electron microscope were dendrites, some of which were post-synaptic to apparent retinal ganglion cell axon terminals. Labelled axons and axon terminals were less frequently encountered. There was considerable overlap between the size distribution of calbindin D28k-immunoreactive neurons and that of GABA-immunoreactive or Nissl stained neurons in the SC. However, using a double fluorescent labelling technique, and examination of the tissue with confocal laser microscopy, no neurons were observed in the hamster SC that showed immunoreactivity for both calbindin and GABA. In this regard, the SC is similar to the mammalian lateral geniculate nucleus and the pretectum, but differs from the neocortex, where calbindin and GABA are colocalized. The demonstration in the SC, as well as other parts of the nervous system, of sub-populations of neurons that contain distinct calcium-binding proteins suggests that these neurons have different functional properties. Correlative studies may clarify the relevance of these cytoplasmic components as cell markers, as well as their different patterns of association with neurotransmitters and peptides.

Summary Peripheral nerve grafts were inserted into the thalamus in 27 Sprague-Dawley rats. From 6 weeks to 15 months later, horseradish peroxidase (HRP) was applied to the extracranial end of each graft and sections of the brains reacted for peroxidase histochemistry. Of the thalamic neurons that were retrogradely labelled with HRP, more than 80% were located in the reticular nucleus of the thalamus (RNT), a distinct group of nerve cells that contain glutamic acid decarboxylase (GAD)-like immunoreactivity and are presumably GABAergic. By combining immunocytochemistry with HRP histochemistry, it was possible to confirm that the RNT neurons that had grown axons into the peripheral nerves grafts retained their GAD-like immunoreactivity. The apparent selectivity in their regenerative responses of RNT neurons to peripheral nerve grafts may relate to special properties of the neurons that did and did not grow into the grafts.

Plasma somatostatin response to food and the administration of the long-acting somatostatin analogue SMS 201–995, as well as pituitary responses to insulin-induced hypoglycemia, growth hormone-releasing hormone (GHRH) and thyrotropin-releasing hormone (TRH), were assessed in a 60- year-old woman with biopsy-proven metastatic somatostatinoma. SMS 201–995 alone did not change plasma somatostatin-like immunoreactivity (SRIF), but levels of low-molecular-weight forms (SRIF- 14 and SRIF-28) more than doubled in response to a standard meal. This postprandial response was not affected by pretreatment with SMS 201–995. Although a growth hormone response to insulin-induced hypoglycemia and supramaximal GHRH was absent, the patient's thyroid-stimulating hormone response to TRH was normal. These results suggest that somatostatin analogues may not influence tumor autonomy and that a SRIF response to food may contribute to early satiety in patients with somatostatinoma. In addition, the long-term use of somatostatin analogues to suppress hormone production by other peptide-secreting tumors may not have predictable results.

This study investigated the association of dietary restraint and disinhibition with self-reported and actual eating behavior, body mass, and hunger. A sample of 124 women were categorized into one of four groups based upon high and low scores on measures of Dietary Restraint and Disinhibition using the Three Factor Eating Questionnaire. Half of the participants in each group consumed a high sugar/high fat chocolate pudding as a dietary preload. All participants were given a meal comprised of a standard macaroni and beef product. The interaction of Dietary Restraint and Disinhibition was related to differences in body mass. The Dietary Restraint factor was related to self-reported pathological eating behavior and influenced both perceived hunger and subjective hunger ratings. However, actual eating behavior measured by calories consumed and rate of intake was unrelated to the Dietary Restraint factor. Disinhibition was associated with excessive eating, an increased rate of eating, self-reports of eating disorder symptomatology, and perceived hunger. Hence, actual eating behavior was significantly influenced by the ingestive motivational factor, Disinhibition, but not by the cognitive factor, Dietary Restraint. These data also suggest that the Disinhibition construct is measuring overeating rather than disinhibited eating which implies the disruption of Dietary Restraint.

Multiple discontinuities are observed in the basal laminas of Schwann cells in mature dystrophic mice. To explore the pathogenesis of this abnormality we have exploited a dystrophic in equilibrium shiverer mouse chimera preparation in which both the basal lamina phenotype and the genotype of myelin-forming Schwann cells can be determined. If the basal lamina abnormality were to arise from an intrinsic deficiency of the dystrophic Schwann cell itself, only those Schwann cells of dystrophic genotype could express the mutant phenotype, whereas the coexisting population of shiverer Schwann cells should express typically normal basal laminas. No such distinction was observed; rather both dystrophic and shiverer Schwann cells were found to express relatively normal basal laminas and two pathogenetic mechanisms remain theoretical possibilities. The dystrophic Schwann cell population may be intrinsically defective but also may be rescued by obtaining the normal product of the dy locus synthesized by the coexisting shiverer cells. Alternatively, an extra Schwann cell deficiency existing within dystrophic mice may be normalized by shiverer cells and the normal intrinsic potential of both dystrophic and shiverer Schwann cells can then be realized. Regardless of the exact mechanism underlying these findings, some extracellularly mediated influence, emanating in vivo from shiverer cells, is capable of ameliorating the basal lamina deficiency typically expressed by dystrophic Schwann cells.

Postweaning development was monitored in domesticated rabbits reared in single- or mixed-sex groups at a commercial farm. The results suggest that sex composition of cage groups had no significant effect on weight gain, feed intake or mortality rates from weaning (35 days) to marketing (93 days). On sacrifice at 93 days, females from single- and mixed-sex groups showed no significant differences in plasma gonadotropin levels (LH and FSH) or weights of paunched carcase, ovaries, uterus, adrenals, kidneys or kidney fat. Evidence for within-cage dominance hierarchies was found at 63 days of age when 46% of the rabbits inspected showed signs of aggressive attack.

Optic nerve transection in adult rats results in the death of approximately 50% of the axotomized retinal ganglion cells (RGCs) by 1 week and nearly 90% by 2 weeks after injury. The capacity of brain-derived neurotrophic factor (BDNF) to prevent this early, severe loss of RGCs was investigated in vivo by intravitreal injections of BDNF [5 micrograms in 5 microliters of bovine serum albumin/phosphate-buffered saline (BSA/PBS)] or vehicle (5 microliters of BSA/PBS). Using quantitative anatomical techniques, we show that (i) all RGCs survived 1 week after a single injection of BDNF at the time of axotomy. (ii) RGC densities decreased in the BDNF-treated retinas by 2 weeks but remained significantly greater than in the untreated controls. (iii) An enhanced RGC survival was obtained with single injections of BDNF from 6 days before to 5 days after axotomy. (iv) Repeated injections resulted in greater numbers of surviving RGCs, an effect that declined to undetectable levels by 6 weeks. (v) There were indications for an endogenous local source of trophic support whose expression was triggered by ocular injury, particularly to the anterior part of the eye. (vi) With multiple BDNF injections, there was profuse axonal sprouting around the optic disc. This remarkable intraretinal growth was not, however, reflected in increased RGC innervation of the peripheral nerve grafts, which are known to facilitate regeneration when used as optic nerve substitutes.

The restoration of connections in the injured central nervous system (CNS) of adult mammals is hindered by the failure of axons to grow back to their natural fields of innervation. Following transection of the optic nerve of adult rodents, the guided regeneration of retinal ganglion cell (RGC) axons along a transplanted segment of peripheral nerve (PN) has shown that these neurones retain their capacities to form well-differentiated synapses in both normal and abnormal targets. The main aim of this review is to describe the anatomical and functional characteristics of some of these connections and to suggest that their terminal distribution and morphology may be the result of a persistence in these targets of molecular determinants that influence normal connectivity in the intact animal.

Summary PC12 cells attach well to plastic culture dishes coated with laminin, collagen, polylysine or a basement membrane extract (2-dimensional substrata) and, in the presence of NGF, extend short neurites within 1–2 days. However, on gels (3-dimensional substrata) reconstituted from a basement membrane extract (RBM), PC12 cells attach extending short processes transiently and within one day, form networks of small aggregates interconnected by process-bearing cells. By 3 days the network collapses into large aggregates that, in media supplemented with NGF, extend a halo of neurites resembling dorsal root ganglia in culture. Time-lapse video recordings indicate that cell motility on RBM gel is accompanied by extensive blebbing as well as extension of processes that attach to and pull together neighbouring cells. These cellular events may contribute to the disruption of the gel underneath aggregates that is apparent when cultures are stained with Coomasie Blue. Ultrastructural studies indicated that aggregates often have zonula adherens-type junctions where cell bodies and processes come in contact. PC12 cells seeded onto gels of laminin alone behave essentially the same as on RBM gels, whereas on collagen gels they behave as on 2-dimensional substrata and extend neurites rather than aggregate. The extent of aggregation increases with greater cell density and is enhanced significantly by NGF. Antisera to NGF reduce the NGF-enhancement of aggregation but do not block aggregation in the absence of NGF. Dibutyryl cAMP or epidermal growth factor, which stimulate process extension and cell division respectively, do not enhance aggregation. However, 3A3, a monoclonal antibody to a laminin/collagen receptor on PC12 cells and antibodies (Fab fragments) to the neural cell adhesion molecule both inhibit cell aggregation.

Summary Synapse formation by retinal ganglion cell axons was sought in the superior colliculus of four adult rats 16–18 months after the optic nerve was transected and replaced by a peripheral nerve graft that guided regenerating RGC axons from the eye to the superior colliculus. The terminals of retinal ganglion cell axons were labelled by intravitreal injections of tritiated amino acids and studied by light and electron microscopic autoradiography. We found that (i) retinal ganglion cell axons had extended from the tips of the peripheral nerve grafts into the superior colliculus for approximately 350 µ,m; (ii) within the superior colliculus, some regenerated retinal ganglion cell axons became ensheathed by CNS myelin; (iii) retinal ganglion cell terminals formed asymmetric synapses with dendrites of neurons in the superficial layers of the superior colliculus, mainly the stratum griseum superficialis.

Summary In adult mice, most nerve fibres in the cervical sympathetic trunk (CST) are unmyelinated whereas a large proportion of sural nerve fibres are myelinated. This study of nerve grafts in syngeneic mice was designed to determine if Schwann cells originating from the unmyelinated CST would produce myelin when in contact with regenerating axons of the sural nerve. Quantitative microscopy of tritiated thymidine-labelled CST segments grafted to unlabelled sural nerve stumps revealed that, one month after grafting, previously unmyelinated grafts contained many myelinated fibres. By phase and electron microscope radioautography, nearly 40% of the myelin-producing cells in the reinnervated graft were shown to have originated in the unmyelinated CST. These findings indicate that Schwann cells originating from unmyelinated fibres are able to differentiate into myelin producing cells.

Summary Beginning prenatally and during the first week after birth, there is normally a loss of axons in rat cervical sympathetic trunk. To test the hypothesis that this spontaneous axonal loss represents a natural process whereby an excessive number of immature preganglionic axons in the cervical sympathetic trunk adapts to the neuronal population in the superior cervical ganglion, the number of nerve cells in the superior cervical ganglion was reduced in newborn rats by administration of nerve growth factor antiserum, 6-hydroxy-dopamine or postganglionic axotomy. Quantitative ultrastructural studies of these animals at later stages of development revealed that, with each method, the number of preganglionic axons and Schwann cells was reduced to nearly one-third of normal. These findings indicate that the superior cervical ganglion plays an important role in the development of the cervical sympathetic trunk. Removal of ganglionic cells causes a retrograde loss of preganglionic fibres. This process probably represents an exaggeration of the normal mechanism for elimination of redundant axons. Because the changes in axonal numbers are associated with similar reductions in the number of Schwann cells, it can also be concluded that postnatal Schwann cell proliferation is influenced by axonal populations.