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J P Max

Publications and source records attributed to J P Max.

At least 19 recordsLinked to original sources
PubMed1999

Dietary preferences of Brattleboro rats correlated with an overexpression of galanin in the hypothalamus.

Galanin (GAL) is a neuropeptide cosynthesized with vasopressin (AVP) in neurons of the hypothalamo-neurohypophysial system. It increases food intake when injected into the brain and elicits an overconsumption of fat. The Brattleboro rat (DI) is genetically unable to produce AVP; the AVP-deficient-producing neurons of the hypothalamo-neurohypophysial system of DI rats are chronically stimulated and DI rats suffer from diabetes insipidus. We studied the central expression of GAL and the dietary preferences in the DI rat. GAL was overexpressed in the hypothalamus of the DI rat. GAL mRNA was higher by 1.8-fold in the supraoptic (P < 0.05) and by four-fold in the paraventricular nuclei (P < 0.001) of male and female DI rats compared with those of control Long Evans (LE) rats. However, GAL mRNA was lower in the arcuate nuclei of DI rats and equal to that of LE rats in the dorsomedian nuclei. We also measured a high preference for a lipid diet (45% of the daily consumption) when DI rats ate from a choice of the three macronutrients. Chronic infusion with deamino-8D-AVP (agonist of AVP V2 receptors) prevented the diabetes insipidus and the chronic stimulation of the hypothalamo-neurohypophysial system of the DI rats. However, the treatment did not suppress the overexpression of GAL, nor did it affect the rats' preference for a lipid diet. We conclude that the DI rat provides a novel animal model in which a spontaneous dietary preference correlates with the overexpression of one of the hypothalamic peptides, GAL.

Animals↗
PubMed1996

Melanin-concentrating hormone is a potent anorectic peptide regulated by food-deprivation and glucopenia in the rat.

Melanin-concentrating hormone is a cyclic nonadecapeptide that is produced almost exclusively in neurons of the lateral hypothalamus and sub zona incerta areas while fibers are widespread in the rat brain. Such a localization strongly suggests that this peptide might participate as neurotransmitter/neuromodulator in the control of feeding behavior. In this study we examined first the influence of rat melanin-concentrating hormone on feeding behavior at different times either in the light or in the dark period (light off at 18.00 h) of the day in fed Wistar rats. Intracerebroventricular injection of rat melanin-concentrating hormone (1-100 ng per rat) at 18.00 h reduced food consumption as early as 2 h after injection and for the next 24 h. In addition, similar anorectic effect was noted after bilateral administration of 1 ng melanin-concentrating hormone into the lateral hypothalamic area at 11.30 h but not at 16.30 h. These findings strongly suggest that rat melanin-concentrating hormone may exert inhibitory control over food intake behavior depending on the circadian rhythm. Second, we investigated the modifications induced by food deprivation/refeeding on melanin-concentrating hormone messenger RNA levels in Wistar rats. Total RNA was isolated from whole hypothalamic dissections and the contents of melanin-concentrating hormone messenger RNA, beta-actin messenger RNA (taken as sample control) and neuropeptide Y messenger RNA (taken as control of food-deprivation paradigms) were assessed by using northern blotting. The time-course of messenger RNA expression was determined in groups of rats deprived for 24, 48 and 72 h and revealed a three-fold induction of melanin-concentrating hormone messenger RNA by 24 and 48 h, with reduced increase at 72 h. As expected, the same treatment led to a three-fold increase in neuropeptide Y messenger RNA content by 48 and 72 h. Refeeding groups of animals for up to 72 h after 24 h of food deprivation resulted in full restoration of melanin-concentrating hormone messenger RNA levels by 24 h. Strikingly, a large range of variations in melanin-concentrating hormone messenger RNA content between individuals was observed in food-deprived versus controls or refed rats suggesting that genetic or environmental factors may alter response in melanin-concentrating hormone gene activity after food deprivation. Finally, we investigated the effects of short-term glucoprivation induced by intraperitoneal administration of either 2-deoxy-D-glucose or insulin on melanin-concentrating hormone messenger RNA expression. A transitory increase in melanin-concentrating hormone messenger RNA content was noted 1 h after 2-deoxy-D-glucose injection while melanin-concentrating hormone messenger RNA levels rose two-fold only 5 h after insulin treatment. These results indicate that 2-deoxy-D-glucose and insulin activate melanin-concentrating hormone gene expression through likely distinct regulatory pathways.

Animals↗
PubMed1994

Increased threshold concentrations of neuropeptide Y for a stimulatory effect on food intake in obese Zucker rats--changes in the microstructure of the feeding behavior.

A central dysregulation of several neuropeptides could be at the origin of the marked hyperphagia of the obese Zucker rat, a well-known animal model used for the study of obesity. Neuropeptide Y (NPY), which strongly stimulates food intake and increases early in life in obese rats, plays a major role in the development of this hyperphagia. The aim of our experiment was to measure the feeding responses of lean (n = 8) and obese (n = 17) male Zucker rats to several doses of exogenous NPY injected in the lateral brain ventricle. We analyzed the microstructure of the rats' feeding behavior with an automatic device for 8 h post-injection. NPY stimulated food intake both in the lean and obese rats in a dose-dependent manner (P < 0.001). However, the minimal effective dose was always 3-4 times greater in the obese rats than in the lean ones (range: 0.43-0.53 vs. 0.12-0.18 microgram/brain; P < 0.001). Meal size, meal duration and time spent eating significantly increased in the lean rats (P < 0.05 or less). The last two parameters also increased in the obese rats but with the highest dose (5 micrograms) only. The obese Zucker rats were therefore less sensitive to NPY than the lean ones, probably because of their already high endogenous NPY levels. The modifications in the eating behavior indicate that NPY could overcome the satiety signals.

Animals↗
PubMed1994

Hypothalamic neuropeptides could mediate the anorectic effects of fenfluramine.

Oxytocin, vasopressin and corticotrophin releasing factor have anorectic properties when injected centrally. We studied the kinetics of these neuropeptides by injecting fenfluramine, a drug which reduces food intake, in Long Evans rats. The drug was injected daily through a double chronic cannula implanted above the paraventricular nucleus of the hypothalamus; the rats had free access to pure macronutrients. The rats lost weight during the treatment. Their total caloric intake decreased mostly because the carbohydrate intake decreased, while the protein intake increased slightly. The synthesis and release of brain oxytocin and vasopressin were increased and the release of corticotrophin releasing factor was stimulated. The neuropeptides could be involved in fenfluramine-triggered mechanisms.

Animals↗
PubMed1994

Macronutrient type independently of energy intake modulates hypothalamic neuropeptide Y in Long-Evans rats.

Neuropeptide Y (NPY) induces a robust feeding response when it is injected in the hypothalamus. It stimulates both carbohydrate and fat intakes. Diets rich in either macronutrient are known to induce obesity and to modify feeding behavior. The aim of the present study was to determine the effects of long-term ingestion of these diets on hypothalamic NPY in relation with food intake and body weight gain and composition. For this purpose, three groups of weanling Long-Evans rats were fed either a well-balanced diet, a high-carbohydrate (HC) diet (high starch plus 25% sucrose solution), or a high-fat (HF) diet during 14 weeks. Body weight and food intake were recorded during this period. At the end of the experiment, NPY was measured in several microdissected brain areas, and some adipose tissues (AT) depots were sampled. HF rats weighed significantly more than the two other groups (p < 0.02). They were also fattier (+ 30-50% in AT weights; p < 0.01). Energy intake (EI) of the HC rats was significantly greater than that of the control (+ 15%; p < 0.02) and HF rats (+ 34%; p < 0.01) during the week preceding killing. EI of HF rats over the whole experiment was lower than that of the two groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Ingestive behaviors of the rat deficient in vasopressin synthesis (Brattleboro strain). Effect of chronic treatment by dDAVP.

Spontaneous manipulator and locomotor activities, food and fluid intake have been recorded from rats suffering from a genetic lack of central vasopressin (VP) synthesis (Brattleboro strain, DI), their heterozygous litter mates (HZ) or Long Evans (LE) rats. The daily patterns of activities did not differ, except for their drinking behavior. This was mainly associated with food intake during the dark period with LE rats but was distributed equally during light and dark periods with DI rats. HZ rats showed a behavioral heterogeneity, some of them following the daily pattern of LE rats, and others, that of DI rats. The daily feeding pattern was identical in the three genotypes but the selection between two isocaloric contrasted diets was different. When they were fed ad lib, HZ and DI rats consumed less carbohydrate than LE rats, the protein intake being unchanged. On the contrary, when the DI rats were only fed during the dark period, they ate more carbohydrate than LE rats. The peripheral infusion of a V2 AVP agonist (dDAVP) restored a normal hydric balance in DI rats but failed to modify the diet selection. These data show that in the rats, the lack of central VP synthesis disturbs both the selection of diets and the efficiency of the satiety signals. These disturbances were unchanged by the peripheral VP treatment which suggested the direct involvement of the central release of the neuropeptide.

Animals↗
PubMed1989

Refeeding after various times of ingestion of a low protein diet: effects on food intake and body weight in rats.

Rats born of protein-deprived mothers were fed on a low protein (LP) diet (5% casein) from weaning. In each time sequence (0, 1, 3, 5, 8 and 16 weeks after weaning), 12 of them were refed on an isocaloric well-balanced diet (18% casein) for 2 weeks. Food intake, body and adipose tissue weights and protein efficiency ratio (PER) were measured in the refed rats as well as in 12 LP rats. At weaning and after one week, refed (RF) rats immediately increased their food intake. This increase was delayed at weeks 3, 5 and 8 occurred during the second week of refeeding only. At week 16, there was a significant decrease during the first week when compared with LP rats. Body weight increased regularly during each refeeding period without any significant augmentation of the proportion of adipose tissue. During all the experiment (except at week 16), PER in the RF group remained high (about 3 g body weight/g protein) during the first week of refeeding, and fell to 2.0-2.5 g/g during the second week. It was particularly significantly greater than that of the LP rats between week 3 and 5 where an important decrease was observed in this group (1.99 +/- 0.36 vs. 3.23 +/- 0.58 g body weight/g protein during the 1-3 weeks period). It appeared therefore that protein restriction during gestation and lactation in dams had no effect on the mechanisms controlling food intake of their offspring at weaning.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1988

The effects of gastric inhibitory polypeptide and insulin on fatty acid uptake in adipose tissue are not mediated through cyclic AMP in lean and obese Zucker rats.

To determine the mechanism by which gastric inhibitory polypeptide (GIP) and insulin stimulate the in vitro fatty acid incorporation into adipose tissue (FIAT), we measured the cyclic AMP variations and FIAT in epididymal fat pads of lean Fa/-- and obese fa/fa Zucker rats. GIP was used at 1, 2 and 4 ng/ml and insulin at a concentration of 100 microU/ml. There was no significant variation of cAMP when FIAT was stimulated either by GIP, either by insulin or by both hormones. There was no correlation at all between FIAT increases and cAMP levels. We conclude that GIP and insulin act through cAMP independent mechanisms in adipose tissue. The modification by GIP of insulin binding to adipocytes or an easier passage of fatty acids through the membrane could constitute alternative solutions for such mechanisms.

Adipose Tissue↗
PubMed1988

Effect of the duration of malnutrition and of nutritional rehabilitation on blood glucose homeostasis and pancreatic hormones in rats.

1. To study the efficiency of rehabilitation after different periods of protein-energy malnutrition, we used as a model preweaning malnourished rats. After weaning, male Wistar rats were fed on a protein-deficient diet (50 g casein/kg) ad lib. for the whole study (DR group) or rehabilitated with normal diet (180 g casein/kg; RR group) from weaning, week 0, or weeks 1, 3, 5, 8 and 16 thereafter. 2. Twelve animals from the DR group were killed at the beginning of each rehabilitation period. The twelve rehabilitated rats were killed after 2 weeks. Body-weight and epididymal adipose tissue weight, blood glucose, plasma immunoreactive insulin (IRI) and immunoreactive glucagon (IRG), and pancreatic contents of IRI and IRG were determined. 3. Food intake of RR rats rose significantly except during the last period where body-weight increased less than that during the previous period. Fat-pad weights increased in the same manner in DR and RR groups. 4. Blood glucose fell and plasma IRG rose significantly without any change in plasma IRI after each rehabilitation period, except during the last period where blood glucose concentrations became stable. Pancreatic IRG and IRI showed the same type of response to those of the plasma. 5. All short-term rehabilitation periods were similarly efficient at producing catch-up growth. High insulin sensitivity of target cells was responsible for good recovery except after long-term malnutrition.

Animals↗
PubMed1988

Effects of somatostatin on the insulin- and gastric inhibitory polypeptide-stimulated fatty acid esterification in rat adipose tissue.

Relations exist between insulin, somatostatin (S) and gastric inhibitory polypeptide (GIP) for the reciprocal control of their secretion but also for their role in lipid metabolism. In the present experiment, we studied the effects of somatostatin on fatty acid incorporation into epididymal adipose tissue (FIAT) of Wistar rats when it was stimulated by insulin and GIP. Cyclic somatostatin-14 was used at physiological (S1 : 50 pg/ml, S2 : 200 pg/ml) and supraphysiological (S3 : 666 pg/ml) concentrations whereas insulin and GIP were used at postprandial levels (100 microU/ml and 2 ng/ml respectively). Results were expressed as percent of basal incorporation (without any hormones). Somatostatin inhibited basal FIAT at all concentrations and totally abolished the insulin-stimulated FIAT (from 106.4 +/- 2.3 per cent with insulin alone to 92.6 +/- 2.5 per cent with S3, P less than 0.001). GIP enhanced the insulin-stimulated FIAT from 106.4 +/- 2.3 per cent to 113 +/- 3.0 per cent (P less than 0.01). On the contrary, when somatostatin was added with GIP and insulin, FIAT decreased to 102.3 +/- 2.5 per cent for S1 (P less than 0.01) and to 98.2 +/- 2.6 per cent for S3 (P less than 0.001). These results indicate that somatostatin totally inhibits the fatty acid esterification induced by insulin and in the same proportions that induced by insulin associated with GIP. Somatostatin is not only an inhibitor of the secretion of these hormones but also a regulator of their biological action in adipose tissue.

Adipose Tissue↗
PubMed1987

Protein-energy malnutrition in pregnant rats improves the adaptation of the endocrine pancreas in malnourished offspring and induces insulin resistance after rehabilitation.

1. In developing countries, malnutrition begins during pregnancy and lactation. Glucose intolerance is a problem of importance during protein-energy malnutrition (PEM). We therefore studied glucose homeostasis in rats weaned from undernourished mothers. 2. On weaning, 156 male Wistar rats, born from deprived mothers (75 g casein/kg diet), were fed ad lib on either a balanced diet (180 g casein/kg; group DR), or a protein-deficient diet (50 g casein/kg; group DD). At seven time intervals (weeks 0, 1, 3, 5, 8, 16 and 23) twelve rats were weighed, fasted overnight and then decapitated. Blood glucose, plasma insulin (IRI) and glucagon (IRG) levels and pancreatic insulin and glucagon contents were determined. 3. In DR and DD rats blood glucose, which was normal at weaning, dropped in the 1st week and then increased slowly. DR rats were hyperglycaemic from week 16. IRI continually increased during the experiment from near-normal values to hyperinsulinic levels in DR rats; in group DD, it remained stable until week 8 before increasing. IRG, which was very low at weaning, increased to normal levels in the 1st week in group DR; in group DD, it fell slightly during the study. Pancreatic hormone contents were much higher than after normal pregnancy and lactation. 4. We compared these results with those of a previous study with rats born from normal mothers: at weaning in the second experiment the rats were already well adapted to malnutrition. The plasma ratio IRI:IRG in DD rats showed two phases of adaptation: weeks 0-5 when glucose homeostasis did not change and weeks 5-23 when it became increasingly normal. At the end of the experiment DR rats still had a lower body-weight than normal rats but were insulin-resistant.

Adaptation, Physiological↗
PubMed1985

Human and animal fat cell size determination using an image analyzing computer.

An automatization of the fat cell's morphological parameters determination with an image analyzing computer is proposed. The results obtained with this technique are compared to results obtained from the usual methods. Combined with frozen cut slices of adipose tissue, this automatized determination of fat cell size is well adapted for the large number of samples necessary for a specialized hospital service.

Adipose Tissue↗
PubMed1985

Progressive adaptation of the endocrine pancreas during long-term protein deficiency in rats: effects on blood glucose homeostasis and on pancreatic insulin, glucagon and somatostatin concentrations.

Blood glucose, plasma insulin and glucagon, as well as pancreatic insulin, glucagon and somatostatin contents, were measured in control (C group, 18% casein), deprived (D group, 5% casein) and pair-fed (PF) rats at seven intervals during 23 wk after weaning (wk 0). In C rats, plasma and pancreatic insulin showed parallel variations, in D rats, plasma insulin increased normally until wk 3 after weaning, dropped from wk 3 to 8 and was higher in wk 16 and 23 than in wk 8, while pancreatic insulin increased linearly after a significant drop between wk 0 and 1. Insulin variations in D rats were related to protein deficiency until wk 5, but only to energy deficiency thereafter. Circulating and pancreatic glucagon dropped identically for the three groups until wk 5: its role in adaptation to malnutrition is quite irrelevant, although a dysregulation of its secretion was noted. Protein-energy malnutrition induced an increase of pancreatic somatostatin content that was due to the energy deficiency. On the basis of the insulin-to-glucagon ratio, three phases of adaptation to protein-energy malnutrition appeared. From wk 0 to 3, the metabolic priority was growth, whereas glucose homeostasis was secondary, accounting for the early hypoglycemia. From wk 3 to 8 survival was the main priority. After wk 8, the various biochemical parameters stabilized, and growth was parallel to that of normal animals. Protein-energy malnutrition was responsible for a dissociated adaptation of pancreatic hormones.

Adaptation, Physiological↗
PubMed1984

Influence of diet composition on obesity, hyperlipemia and liver steatosis in Zucker fa/fa rats pair-fed with Zucker Fa/- rats.

The effect of a four-week experiment on ten fa/fa Zucker rats (aged seven weeks at the beginning) fed on a lipid-rich diet (HL: 31 per cent w/w lipids, 45.6 per cent starch) was compared to that of a control diet (C: 10 per cent lipids, 66 per cent starch) on control Fa/- rats using a special pair-feeding apparatus that made it possible to obtain an identical intake rhythm. Energy level of the intake was significantly higher for the HL diet than for the C diet. At the end of the experiment, fa/fa rats remained obese and hyperlipemic, and still showed liver steatosis. With equal energy levels ingested, the obesity of fa/fa rats was comparable for both diets; hypertriglyceridemia and hypercholesterolemia were identical for both diets. When compared to the C diet, the HL diet modified neither their obesity nor their hyperlipemia. Obese rat liver on the HL diet showed lower levels for triacylglycerols, cholesterol, GGT, ALT, LDH and aldolase activities, while hepatic glycerol kinase and AST activities were higher than and comparable to, respectively, the C diet. Thus the HL diet led to a decreased liver steatosis for fa/fa rats as compared to the C diet.

Animals↗
PubMed1983

Gastric inhibitory polypeptide enhancement of the insulin effect on fatty acid incorporation into adipose tissue in the rat.

The influence of gastric inhibitory polypeptide (GIP) on fatty acid incorporation into adipose tissue (FIAT) was studied in the rat on epididymal fat pads at concentrations amounting to 1, 2 and 4 ng/ml. Without insulin in the incubation medium, GIP induced a slight though significant FIAT decrease with a maximum of 9% for 2 ng/ml concentration. In the presence of rat insulin (100 microU/ml), it significantly enhanced the insulin-induced FIAT increase, that progressed from 106.4% of the basal value to 110.5% for 1 ng/ml concentration (P less than 0.025) and to 118.2% for 4 ng/ml concentration (P less than 0.0025). The existence of such a phenomenon as well as that of an hyperactive enteroinsular axis in obese subjects could represent two important factors in the development of obesity.

Adipose Tissue↗