Comprehensive Physiology Wiley Online Library

Central Nervous System Control of Nutrient Homeostasis

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Abstract

The sections in this article are:

1 Central Nervous System Control of Food Intake and Body Weight
1.1 History
1.2 Set‐Point Hypothesis
1.3 Control of Food Intake
1.4 Neuropeptides as Satiety Factors
1.5 Neuropeptides That Increase Meal Size
1.6 Central Neural Circuits and Aminergic Transmitters
1.7 Afferent Inputs to Hypothalamus Related to Feeding
2 Central Nervous System Control of Glucose Homeostasis
2.1 Overview
2.2 Overnight Fast
2.3 Plasma Glucose Regulation During Meals
2.4 Plasma Glucose Regulation During Exercise
2.5 Stress Hyperglycemia
2.6 Central Mechanisms for Glucose Sensing and Regulation
2.7 CNS Effects of Neuropeptides on Plasma Glucose
3 Neuroendocrine Effector Organs for Metabolic Regulation
3.1 Endocrine Pancreas
3.2 Liver
3.3 Adipose Tissue
3.4 Skeletal Muscle
4 Conclusions
Figure 1. Figure 1.

Spontaneous reregulation of body weight by free‐feeding rats. Control group of free‐feeding animals (•) compared with 3 tube‐fed groups [pair fed (Δ), overfed 50% of calories (▴), and underfed 20% of calories (○)]. Note return to average weight at end of tube‐feeding period (arrow).

Adapted from Bernstein, Porte, Woods, et al. 56
Figure 2. Figure 2.

Summary model for regulation of food intake and body weight. Food intake modulated by hedonic qualities and gastroenteropancreatic (GEP) hormones. This regulation is modified by signal (hypothesized to be insulin) from adipose mass. CCK, cholecystokinin; CSF, cerebrospinal fluid.

From Porte and Woods 591
Figure 3. Figure 3.

Simplified model of basal glucose regulation that emphasizes critical role of endocrine pancreas as glucose sensor. Neuroendocrine factors are superimposed on this feedback loop. +, Stimulatory; −, inhibitory. NE, norepinephrine; E, epinephrine.

From Woods, Smith, and Porte 826
Figure 4. Figure 4.

Islet as metabolic integrator. GIP, gastrointestinal inhibitory polypeptide.

From Woods, Smith, and Porte 826
Figure 5. Figure 5.

Effects of central peptides on glucose regulation. GRP, gastrin‐releasing peptide; TRF, thyrotropin‐releasing factor; SS, somatostatin; FFA, free fatty acids; AA, amino acids; ODT8‐SS, Des‐Trp‐somatostatin.

From Brown 100


Figure 1.

Spontaneous reregulation of body weight by free‐feeding rats. Control group of free‐feeding animals (•) compared with 3 tube‐fed groups [pair fed (Δ), overfed 50% of calories (▴), and underfed 20% of calories (○)]. Note return to average weight at end of tube‐feeding period (arrow).

Adapted from Bernstein, Porte, Woods, et al. 56


Figure 2.

Summary model for regulation of food intake and body weight. Food intake modulated by hedonic qualities and gastroenteropancreatic (GEP) hormones. This regulation is modified by signal (hypothesized to be insulin) from adipose mass. CCK, cholecystokinin; CSF, cerebrospinal fluid.

From Porte and Woods 591


Figure 3.

Simplified model of basal glucose regulation that emphasizes critical role of endocrine pancreas as glucose sensor. Neuroendocrine factors are superimposed on this feedback loop. +, Stimulatory; −, inhibitory. NE, norepinephrine; E, epinephrine.

From Woods, Smith, and Porte 826


Figure 4.

Islet as metabolic integrator. GIP, gastrointestinal inhibitory polypeptide.

From Woods, Smith, and Porte 826


Figure 5.

Effects of central peptides on glucose regulation. GRP, gastrin‐releasing peptide; TRF, thyrotropin‐releasing factor; SS, somatostatin; FFA, free fatty acids; AA, amino acids; ODT8‐SS, Des‐Trp‐somatostatin.

From Brown 100
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Stephen C. Woods, Gerald J. Taborsky, Daniel Porte. Central Nervous System Control of Nutrient Homeostasis. Compr Physiol 2011, Supplement 4: Handbook of Physiology, The Nervous System, Intrinsic Regulatory Systems of the Brain: 365-411. First published in print 1986. doi: 10.1002/cphy.cp010407