Insulin receptors in the central nervous system: Localization, signalling mechanisms and functional aspects

Unger, J.; Livingston, James N.; Moss, Anne

doi:10.1016/0301-0082(91)90015-s

Cited by 370 publications

(236 citation statements)

References 150 publications

Supporting

Mentioning

213

Contrasting

Unclassified

Order By: Relevance

“…Therefore, the effects of insulin in the hypothalamus could be involved in the reaction in the periphery. This hypothesis is supported by studies in animals, which have revealed that the hypothalamus is crucial to the regulation of peripheral insulin action, especially in the liver [6,26,27], as well as pointing to the wellknown abundance of insulin receptors in this area [28,29].…”

Section: Discussionmentioning

confidence: 76%

Nasal insulin changes peripheral insulin sensitivity simultaneously with altered activity in homeostatic and reward-related human brain regions

et al. 2012

View full text Add to dashboard Cite

Aims/hypothesis Impaired insulin sensitivity is a major factor leading to type 2 diabetes. Animal studies suggest that the brain is involved in the regulation of insulin sensitivity. We investigated whether insulin action in the human brain regulates peripheral insulin sensitivity and examined which brain areas are involved. Methods Insulin and placebo were given intranasally. Plasma glucose, insulin and C-peptide were measured in 103 participants at 0, 30 and 60 min. A subgroup (n012) was also studied with functional MRI, and blood sampling at 0, 30 and 120 min. For each time-point, the HOMA of insulin resistance (HOMA-IR) was calculated as an inverse estimate of peripheral insulin sensitivity.

show abstract

Section: Discussionmentioning

confidence: 76%

Nasal insulin changes peripheral insulin sensitivity simultaneously with altered activity in homeostatic and reward-related human brain regions

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Its formation relies primarily on Brain insulin signaling in obesity M Hallschmid et al hippocampal structures and adjacent cortices 18 where brain insulin receptors are predominantly found. 28 In these structures, insulin increases long-term potentiation and promotes neuronal outgrowth, that is, plastic mechanisms supposed to underlie memory functions at the neuronal level. 27 The slow onset of memory enhancement by intranasal insulin in the absence of acute effects speaks for the involvement of gradual plastic neuronal changes.…”

Section: Discussionmentioning

confidence: 99%

Obese men respond to cognitive but not to catabolic brain insulin signaling

et al. 2007

View full text Add to dashboard Cite

Context and objective: Insulin acts in the brain to reduce food intake and body weight and is considered a major adiposity signal in energy homeostasis. In normal-weight men, intranasal insulin administration reduces body fat and improves declarative memory. The present experiments aimed to generalize these findings to obese patients, with a view to evaluate the therapeutic potential of the compound. Design, subjects and measurements: Insulin and placebo, respectively, were intranasally administered four times a day (amounting to 160 IU day À1 ) over 8 weeks to two groups of 15 obese men each. Results: Contrasting with the catabolic effects in normal-weight men, insulin treatment did not induce any significant reduction of body weight (P40.50) and body fat (P40.44) in the obese subjects. However, in accordance with the effects in normalweight men, declarative memory and mood were improved (Po0.05) and hypothalamic-pituitary-adrenal axis activity as assessed by circulating ACTH (Po0.01) and cortisol levels (Po0.04) was reduced. Conclusions: Our results indicate that in obese men, intranasal insulin is functionally active in the central nervous system but fails to affect the neuronal networks critically involved in body weight regulation. We conclude that obesity in men is associated with central nervous resistance to the adiposity signal insulin. This defect likely contributes to the persistence of obesity in spite of elevated levels of circulating insulin in obese patients.

show abstract

“…It can be a result of differences in structure of receptors originating from various tissues. The brain receptor is a bit smaller molecule and this distinction arises from differences in N-linked glycosylation (Unger et al, 1991a;Gammeltoft et al, 1984). However, besides described differences in the characteristics of brain and liver membrane receptors, in the light of the present paper, it can be stated both their ability to changing in various circumstances and the regulatory effect of a diet on them.…”

Section: Resultsmentioning

confidence: 61%

High-carbohydrate and high-protein diets alter liver and brain insulin receptors in rats

Maćkowiak¹,

Ładoń²,

Nogowski³

et al. 1993

J. Anim. Feed Sci.

View full text Add to dashboard Cite

Insulin receptors of liver and brain plasma membranes were investigated in rats kept on standard (S), high-carbohydrate (HC) and high-protein (HP) diets. Both liver and brain show similar tendency to reduce number of high affinity receptors and their affinity to the hormone in rats fed a HP diet. After a HC diet the effects seem to be opposite. Animals show nearly the same number of receptors as in the control group but the affinity of insulin binding to liver -but not brain plasma membranes is enhanced.

show abstract

Insulin receptors in the central nervous system: Localization, signalling mechanisms and functional aspects

Cited by 370 publications

References 150 publications

Nasal insulin changes peripheral insulin sensitivity simultaneously with altered activity in homeostatic and reward-related human brain regions

Nasal insulin changes peripheral insulin sensitivity simultaneously with altered activity in homeostatic and reward-related human brain regions

Obese men respond to cognitive but not to catabolic brain insulin signaling

High-carbohydrate and high-protein diets alter liver and brain insulin receptors in rats

Contact Info

Product

Resources

About