Glucocorticoids and insulin: reciprocal signals for energy balance

1995 ◽  
Vol 268 (1) ◽  
pp. R142-R149 ◽  
Author(s):  
A. M. Strack ◽  
R. J. Sebastian ◽  
M. W. Schwartz ◽  
M. F. Dallman
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Diabetic Rats ◽  
Energy Gain ◽  
Energy Stores ◽  
The Central Nervous System ◽  
Streptozotocin Induced Diabetes ◽  
Term Energy

Signals that regulate long-term energy balance have been difficult to identify. Increasingly strong evidence indicates that insulin, acting on the central nervous system in part through its effect on neuropeptide Y (NPY), inhibits food intake. We hypothesized that corticosteroids and insulin might serve as interacting, reciprocal signals for energy balance, acting on energy acquisition, in part through their effects on hypothalamic NPY, as well as on energy stores. Because glucocorticoids also stimulate insulin secretion, their role is normally obscured. Glucocorticoids and insulin were clamped in adrenalectomized rats with steroid replacement and streptozotocin-induced diabetes. Glucocorticoids stimulated and insulin inhibited NPY mRNA and food intake. Glucocorticoids inhibited and insulin increased energy gain as determined by the change in body weight. When adrenalectomized diabetic rats were treated, corticosterone stimulated and insulin inhibited food intake, and, respectively, inhibited and increased overall energy gain. More than 50% of the variance was explained by regression analysis of the two hormones on food intake and body weight. Thus glucocorticoids and insulin are major, antagonistic, long-term regulators of energy balance. The effects of corticosterone and insulin on food intake may be mediated, in part, through regulation of hypothalamic NPY synthesis and secretion.

The role of exercise in thermogenesis and energy balance

1989 ◽  
Vol 67 (4) ◽  
pp. 402-409 ◽  
Author(s):  
Denis Richard ◽  
Serge Rivest
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Exercise Training ◽  
Female Rats ◽  
Male Rats ◽  
Brown Adipose ◽  
Term Energy

The role of exercise training in energy balance has been reviewed. Recent well-conducted studies showed that exercise may increase energy expenditure not only during the period of exercise itself but during the postexercise period as well. This notion of excess postexercise oxygen consumption (EPOC), which has been a controversial issue for many years, is now becoming a generally well-accepted concept, the consensus being that EPOC takes place following prolonged and strenuous exercise bouts. Besides, the role of EPOC in long-term energy balance remains to be determined. Long-term energy balance studies carried out in rats show that exercise affects energy balance by altering food intake and promoting energy expenditure. In male rats exercise causes a marked decrease in energy intake which contributes, in association with the expenditure of exercise itself, to retard lean and fat tissue growth. From the suppressed deposition of lean body mass, decreases in basal metabolic rate can be predicted in males. In female rats, exercise does not affect food intake; the lower energy gain of exercise-trained females results from the elevated expenditure rate associated with exercise itself. In both male and female rats, there is no evidence that exercise training affects energy expenditure other than during exercise itself unless the habitual feeding pattern of the rats is radically modified. The interactive effects of diet and exercise, which have to be further investigated in long-term energy balance, emerge as a promising area of research.Key words: exercise training, nutritional energetics, brown adipose tissue, diet-induced thermogenesis, body composition.

Central Histamine, the H3-Receptor and Obesity Therapy

2019 ◽  
Vol 18 (7) ◽  
pp. 516-522
Author(s):  
Néstor F. Díaz ◽  
Héctor Flores-Herrera ◽  
Guadalupe García-López ◽  
Anayansi Molina-Hernández
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Receptor Activation ◽  
Receptor Ligands ◽  
Histaminergic System ◽  
H3 Receptor ◽  
Weight One ◽  
The Central Nervous System

The brain histaminergic system plays a pivotal role in energy homeostasis, through H1- receptor activation, it increases the hypothalamic release of histamine that decreases food intake and reduces body weight. One way to increase the release of hypothalamic histamine is through the use of antagonist/inverse agonist for the H3-receptor. Histamine H3-receptors are auto-receptors and heteroreceptors located on the presynaptic membranes and cell soma of neurons, where they negatively regulate the synthesis and release of histamine and other neurotransmitters in the central nervous system. Although several compounds acting as H3-receptor antagonist/inverse agonists have been developed, conflicting results have been reported and only one has been tested as anti-obesity in humans. Animal studies revealed the opposite effect in food intake, energy expeditor, and body weight, depending on the drug, spice, and route of administration, among others. The present review will explore the state of art on the effects of H3-receptor ligands on appetite and body-weight, going through the following: a brief overview of the circuit involved in the control of food intake and energy homeostasis, the participation of the histaminergic system in food intake and body weight, and the H3-receptor as a potential therapeutic target for obesity.

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

2016 ◽  
Vol 5 (06) ◽  
pp. 4641 ◽  
Author(s):  
Adel Abdel Moneim* ◽  
Sanaa M. Abd El-Twab ◽  
Mohamed B. Ashour ◽  
Ahmed I. Yousef
Keyword(s):  
Body Weight ◽  
Gallic Acid ◽  
Protein Profile ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Hypoglycemic Agents ◽  
Protective Effects ◽  
Coumaric Acid ◽  
Experimental Type

The goal of diabetes treatment is primarily to save life and alleviate symptoms and secondary to prevent long-term diabetic complications resulting from hyperglycemia. Thus, our present investigation was designed to evaluate the hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin (NA/STZ)-induced diabetic rats. Experimental type 2 diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (65 mg/kg b.wt.), after 15 min of i.p. injection of NA (120 mg/kg b.wt.). Gallic acid and p-coumaric acid were orally administered to diabetic rats at a dose of 20, 40 mg/kg b.wt./day, respectively, for 6 weeks. Body weight, serum glucose, protein profile, liver function enzymes and kidney function indicators was assayed. Treatment with either gallic acid or p-coumaric acid significantly ameliorated the elevated levels of glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and uric acid. Both compounds were also found to restore total protein, albumin, and globulin as well as body weight of diabetic rats to near normal values. It can conclude that both gallic acid and p-coumaric acid have potent hypoglycemic and hepato-renal protective effects in diabetic rats. Therefore, our results suggest promising hypoglycemic agents that can attenuate the progression of diabetic hepatopathy and nephropathy.

Secretin as a satiation whisperer with the potential to turn into an obesity-curbing knight

Endocrinology ◽  
2021 ◽  
Author(s):  
Katharina Schnabl ◽  
Yongguo Li ◽  
Mueez U-Din ◽  
Martin Klingenspor
Keyword(s):  
Bariatric Surgery ◽  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Weight Control ◽  
Therapeutic Potential ◽  
Physiological Mechanism ◽  
Gut Hormones ◽  
Metabolic Effects ◽  
Beneficial Effects

Abstract The obesity pandemic requires effective preventative and therapeutic intervention strategies. Successful and sustained obesity treatment is currently limited to bariatric surgery. Modulating the release of gut hormones is considered promising to mimic bariatric surgery with its beneficial effects on food intake, body weight and blood glucose levels. The gut peptide secretin was the first molecule to be termed a hormone; nevertheless, it only recently has been established as a legitimate anorexigenic peptide. In contrast to gut hormones that crosstalk with the brain either directly or by afferent neuronal projections, secretin mediates meal-associated brown fat thermogenesis to induce meal termination, thereby qualifying this physiological mechanism as an attractive, peripheral target for the treatment of obesity. In this perspective, it is of pivotal interest to deepen our yet superficial knowledge on the physiological roles of secretin as well as meal-associated thermogenesis in energy balance and body weight regulation. Of note, the emerging differences between meal-associated thermogenesis and cold-induced thermogenesis must be taken into account. In fact, there is no correlation between these two entities. In addition, the investigation of potential effects of secretin in hedonic-driven food intake, bariatric surgery as well as chronic treatment using suitable application strategies to overcome pharmacokinetic limitations will provide further insight into its potential to influence energy balance. The aim of this article is to review the facts on secretin’s metabolic effects, address prevailing gaps in our knowledge, and provide an overview on the opportunities and challenges of the therapeutic potential of secretin in body weight control.

scholarly journals Assessment of anti-diabetic activity of alcoholic and hydro-alcoholic extract of Terminalia arjuna & Syzygium cumini in streptozotocin-induced diabetes in Wistar rats

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 1870-1882
Author(s):  
Takru Harshit ◽  
Dixit Praveen K ◽  
Kumar Kapil ◽  
Nagarajan K
Keyword(s):  
Body Weight ◽  
Glucose Level ◽  
Biochemical Parameters ◽  
Wistar Rats ◽  
Diabetic Rats ◽  
Terminalia Arjuna ◽  
Alcoholic Extract ◽  
Syzygium Cumini ◽  
Liver And Pancreas ◽  
Streptozotocin Induced Diabetes

We aimed to evaluate the effect of anti-diabetic activity of Terminalia arjuna, and Syzygium cumini extracts in Streptozotocin (STZ) induced diabetes in Wistar rats. STZ (55mg/kg) followed by nicotinamide (100mg/kg) was given to rats by intraperitoneal route to induce diabetes. Oral administration of alcoholic and hydro-alcoholic extracts of T. arjuna (TAAE) (250mg/kg and 500mg/kg), S. cumini (SCAE) (200mg/kg and 400mg/kg) and their composite extract were given to rats along with standard anti-diabetic drug Glibenclamide (5mg/kg). We evaluated body weight, glucose level, lipid profile and biochemical parameters in STZ induced diabetic rats. Also, histopathological studied were done in liver, kidney and pancreatic tissues of rats. Our finding revealed that TAAE and TAHE at 250mg/kg b.w. and 500mg/kg b.w., SCAE and SCHE at 400mg/kg b.w. and combination of TAAE (250mg/kg b.w.)+SCAE (400mg/kg b.w.) had a positive effect in lowering the blood glucose level and body weight on 28th day as compared to the initial observation on 0th day and also restored all the biochemical parameters such as LDL, VLDL, triglycerides and total Cholesterol and HDL towards the normal levels as well as histopathological improvement in Kidney, Liver and Pancreas. Data analysis showed that composite extract of TAAE (250mg/kg) and SCAE (400mg/kg ) improved diabetic consequences more effectively than composite extract of TAHE (500mg/kg) and SCHE (400mg/kg). TAAE and SCHE, in combination, demonstrate as a potential therapeutic agent against diabetes.

scholarly journals Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Positive Energy ◽  
Chow Diet ◽  
Chromatin Regulator ◽  
Positive Energy Balance ◽  
The Impact ◽  
Deficient Mice

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.

Food intake and gastric emptying in rats with streptozotocin-induced diabetes

1984 ◽  
Vol 247 (6) ◽  
pp. R1054-R1061 ◽  
Author(s):  
J. G. Granneman ◽  
E. M. Stricker
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Carbohydrate ◽  
Streptozotocin Induced Diabetes

Recent studies suggest that the rate of nutrient transit through the upper gastrointestract may provide cues that are important to the control of food intake. We examined gastrointestinal function in rats with streptozotocin-induced diabetes and related these findings to concomitant changes in food intake. Control and diabetic rats were adapted to one of two isocaloric diets either high in carbohydrate or fat. Control rats ate similar amounts of each diet. In contrast, diabetic animals fed high-carbohydrate diet were hyperphagic, whereas those fed low-carbohydrate diet ate normal amounts of food. Gastric emptying, intestinal mass, disaccharidase activity, and glucose absorption were increased in normophagic diabetic rats fed a low-carbohydrate diet. Feeding diabetic rats high-carbohydrate diet potentiated each of these effects, and food intake was highly correlated with rate of gastric emptying. These and other results indicate that diabetes enhances gastric emptying and intestinal carbohydrate digestion and absorption, even in the absence of hyperphagia. Consequently, the hyperphagia of diabetic rats may be in part a behavioral response to a greatly accelerated clearance of nutrients from the upper gastrointestinal tract that occurs when these animals are fed diets rich in carbohydrate.

Long-term energy balance in child-bearing Gambian women

1981 ◽  
Vol 34 (12) ◽  
pp. 2790-2799 ◽  
Author(s):  
A M Prentice ◽  
R G Whitehead ◽  
S B Roberts ◽  
A A Paul
Keyword(s):  
Energy Balance ◽  
Child Bearing ◽  
Term Energy

Hypothalamic paraventricular nucleus lesions do not prevent anorectic effect of exercise in male rats

1990 ◽  
Vol 259 (3) ◽  
pp. R579-R584 ◽  
Author(s):  
S. Rivest ◽  
D. Richard
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Paraventricular Nucleus ◽  
Wistar Rats ◽  
Energy Gain ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Serum Corticosterone ◽  
Male Wistar Rats

The effects of a hypothalamic paraventricular nucleus (PVN) lesion on energy balance were investigated in exercise-trained rats. Male Wistar rats weighing initially 250 g were divided into four groups. Two groups of rats underwent a bilateral PVN lesion, whereas the two remaining groups were sham operated. The PVN lesions were done electrolytically. One group from each surgical treatment was exercised, while the other group was kept in sedentary conditions. Rats were exercised on a rodent motor-driven treadmill at moderate intensity, 1 h/day for 21 consecutive days. Food intake and body weight were measured each day during the study. At the end of the treatment period, rats were killed, and carcasses were analyzed for their energy content. Serum corticosterone was measured by a competitive protein-binding assay. Energy gain and energy intake were lower in exercised rats than in sedentary controls, regardless of whether they were sham or PVN lesioned. Concurrently, there was no difference in the energy gain between PVN-lesioned and sham-operated rats, despite the fact that PVN-lesioned rats ended the experiment with a larger body weight than the sham-lesioned animals. Serum corticosterone levels were lower in PVN-lesioned rats than in sham-lesioned rats. In conclusion, the present results indicate that the PVN, the hypothalamic nucleus predominantly controlling the pituitary-adrenal axis activity, is not a prominent structure in the regulation of energy balance in exercised male Wistar rats.

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