Is There Appetite after GLP‐1 and PACAP?

Christophe, Jean

doi:10.1111/j.1749-6632.1998.tb11192.x

Cited by 19 publications

(4 citation statements)

References 98 publications

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“…These alarin-inducing effects may be blocked by co-treatment of alarin antagonist ala6-25Cys (SSPFPPRPTRAGRETQLLRSC), which is eliminated the first 5 amino acids from alarin (APAHRSSPFPPRPTRAGRETQLLRS). Ala6-25Cys can antagonize the promoting effects of alarin on food intake and luteinizing hormone secretion [ 17 , 18 ]. These results suggest that central administration of alarin enhances glucose uptake of the skeletal muscles.…”

Section: Discussionmentioning

confidence: 99%

Intracerebroventricular Injection of Alarin Increased Glucose Uptake in Skeletal Muscle of Diabetic Rats

Zhang

Sheng

et al. 2015

PLoS ONE

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In order to investigate the central effect of alarin on glucose uptake, we administered alarin and/ or its inhibitor, ala6-25Cys into the cerebral ventricles of the type 2 diabetic rats. Then the relative parameters about glucose uptake in skeletal muscles were measured. We found that central treatment with alarin significantly increased the food intake, body weight and glucose infusion rates in hyperinsulinemic euglycemic clamp tests of the animals. Besides, the treatment also enhanced 2-deoxy-[3H]-D-glucose uptake, vesicle-associated membrane protein 2 contents, glucose transporter 4 protein and mRNA expression, as well as pAktThr308, pAktSer473 and total Akt levels in muscle cells, but reduced plasma glucose and insulin levels of the rats. All of the alarin-inducing events may be antagonised by central injection of ala6-25Cys. These results suggest that central administration of alarin stimulates glucose uptake mediated by activation of Akt signal pathway in type 2 diabetic animals.

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Section: Discussionmentioning

confidence: 99%

Intracerebroventricular Injection of Alarin Increased Glucose Uptake in Skeletal Muscle of Diabetic Rats

Zhang

Sheng

et al. 2015

PLoS ONE

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“…Could such an effect be involved in the decrease in body weight occurring in obese Zucker rats, receiving oligofructose in their diet? Or is the effect of on dietary intake linked to GLP-1 production and secretion, since GLP-1 has been proposed as a satietogenic peptide (Christophe, 1998)?…”

Section: Discussionmentioning

confidence: 99%

Inulin and oligofructose modulate lipid metabolism in animals: review of biochemical events and future prospects

Delzenne

Daubioul²,

Neyrinck³

et al. 2002

Br J Nutr

179

105

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Inulin and oligofructose, besides their effect on the gastro-intestinal tract, are also able to exert 'systemic' effect, namely by modifying the hepatic metabolism of lipids in several animal models. Feeding male Wistar rats on a carbohydrate-rich diet containing 10 % inulin or oligofructose significantly lowers serum triacylglycerol (TAG) and phospholipid concentrations. A lower hepatic lipogenesis, through a coordinate reduction of the activity and mRNA of lipogenic enzymes is a key event in the reduction of very low-density lipoprotein-TAG secretion by oligofructose. Oligofructose is also able to counteract triglyceride metabolism disorder occurring through dietary manipulation in animals, and sometimes independently on lipogenesis modulation: oligofructose reduces post-prandial triglyceridemia by 50 % and avoids the increase in serum free cholesterol level occurring in rats fed a Western-type high fat diet. Oligofructose protects rats against liver TAG accumulation (steatosis) induced by fructose, or occurring in obese Zucker fa/fa rats. The protective effect of dietary inulin and oligofructose on steatosis in animals, would be interesting, if confirmed in humans, since steatosis is one of the most frequent liver disorders, occurring together with the plurimetabolic syndrome, in overweight people. The panel of putative mediators of the systemic effects of inulin and oligofructose consists in either modifications in glucose/insulin homeostasis, the end-products of their colonic fermentation (i.e. propionate) reaching the liver by the portal vein, incretins and/or the availability of other nutrients. The identification of the key mediators of the systemic effects of inulin and oligofructose is the key to identify target function(s) (or dysfunction(s)), and finally individuals who would take an advantage of increasing their dietary intake.

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“…GLP‐1 lies upstream to insulin as it stimulates insulin secretion from pancreatic β‐cells (Perry and Grieg, 2003). GLP‐1 and its GLP‐1 receptor are expressed in other regions of the brain such as the hippocampus (Jin et al, 1988; Alvarez et al, 1996; Merchenthaler et al, 1999), suggesting that GLP‐1 acts more than just on the hypothalamus to suppress food intake (Christophe, 1998). According to the During et al (2003) study, the intracerebroventrical infusion of GLP‐1 or the conserved nine‐amino acid N‐terminal domain of the protein, Ser(2)exendin (1‐9) or the intranasal infusion of Ser(2)exedin (1‐9), enhanced associative and spatial memory.…”

Section: Whole Body Metabolism and Cognitive Functionmentioning

confidence: 99%

Revenge of the “Sit”: How lifestyle impacts neuronal and cognitive health through molecular systems that interface energy metabolism with neuronal plasticity

Vaynman

Gómez‐Pinilla

2006

J of Neuroscience Research

259

163

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Exercise, a behavior that is inherently associated with energy metabolism, impacts the molecular systems important for synaptic plasticity and learning and memory. This implies that a close association must exist between these systems to ensure proper neuronal function. This review emphasizes the ability of exercise and other lifestyle implementations that modulate energy metabolism, such as diet, to impact brain function. Mechanisms believed to interface metabolism and cognition seem to play a critical role with the brain derived neurotrophic factor (BDNF) system. Behaviors concerned with activity and metabolism may have developed simultaneously and interdependently during evolution to determine the influence of exercise and diet on cognition. A look into our evolutionary past indicates that our genome remains unchanged from the times of our hunter-gatherer ancestors, whose active lifestyle predominated throughout almost 100% of humankind's existence. Consequently, the sedentary lifestyle and eating behaviors enabled by the comforts of technologic progress may be reaping "revenge" on the health of both our bodies and brains. In the 21st century we are confronted by the ever-increasing incidence of metabolic disorders in both the adult and child population. The ability of exercise and diet to impact systems that promote cell survival and plasticity may be applicable for combating the deleterious effects of disease and ageing on brain health and cognition.

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Is There Appetite after GLP‐1 and PACAP?

Cited by 19 publications

References 98 publications

Intracerebroventricular Injection of Alarin Increased Glucose Uptake in Skeletal Muscle of Diabetic Rats

Intracerebroventricular Injection of Alarin Increased Glucose Uptake in Skeletal Muscle of Diabetic Rats

Inulin and oligofructose modulate lipid metabolism in animals: review of biochemical events and future prospects

Revenge of the “Sit”: How lifestyle impacts neuronal and cognitive health through molecular systems that interface energy metabolism with neuronal plasticity

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