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Physiological Endocrine Control of Energy Homeostasis and Postprandial Blood Glucose Levels

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Physiological Endocrine Control of Energy Homeostasis and Postprandial Blood Glucose Levels European Review for Medical and Pharmacological Sciences 2005; 9: 75-92 Physiological endocrine control of energy homeostasis and postprandial blood glucose levels JUAN J. GAGLIARDINO CENEXA – Center of Experimental and Applied Endocrinology (National University of La Plata, National Research Council, PAHO/WHO Collaborating Center) School of Medical Sciences – La Plata (Argentina) Abstract. – The aim of this review is to Various studies have emphasized the im- analyze the different components and the feed- portance of postprandial hyperglycemia, back mechanisms involved in the normal con- since its association with fatal and nonfatal trol of energy homeostasis and postprandial cardiovascular events is greater than that of blood glucose levels. Such control involves ex- 3 ogenous and endogenous factors: while the fasting hyperglycemia , and even moderate former include quantity and quality of food in- increased levels constitute a risk factor4. The take, the latter involve the balance of glucose risk increases when postprandial hyper- intestinal absorption (postprandial period), glu- glycemia associates with postprandial hyper- cose production and release by the liver and its lipemia; hyperglycemia increases lipid peroxi- consumption by peripheral tissues. Adequate dation, thus increasing lipoprotein athero- secretion and peripheral metabolic effects of insulin play a key role in the control of both genic capacity and decreasing plasma antioxi- 5 processes. Insulin secretion is controlled by dants . Presumably, the higher the glycemic the level of circulating substrates and by gas- increment the higher the decrease of antioxi- trointestinal hormones. The mechanism for the dants will be5. Screening is essential in people immediate control of blood glucose levels is with diabetes presenting fasting glycemia and modulated by energy homeostasis, with the HbA1c levels within normal range, and participation of the above mentioned hormones 6 and others produced at the classical endocrine markedly increased postprandial glycemia . system and adipose tissue, whose actions inte- The regulation of postprandial glycemia is grate at the central nervous system. The alter- complex, and the magnitude of glycemic vari- ation of such delicate mechanism of control ations depends on multiple factors, namely, causes diseases such as diabetes; therefore, food composition, the action of gastrointesti- identification of the multiple components of nal hormones and digestive enzymes, insulin this mechanism and comprehension of its nor- secretion, enhancement or inhibition of he- mal function would facilitate the selection of ef- fective strategies for diabetes prevention and patic glucose production, and peripheral glu- treatment. cose uptake. These factors act during food in- take, together with other factors acting dur- Key Words: ing the day to keep an adequate balance be- Energy homeostasis, Postprandial blood glucose tween intake and total caloric consumption levels, Diabetes, Neuroendocrine control. (energy balance) (Figure 1). The regulation of energy balance is impor- tant because the volume and composition of each food varies considerably from day to day and person to person; the absence of en- Introduction ergy balance could result in the uncoupling of energy intake and caloric consumption. To Near normoglycemia is one of the main explain this model of energy homeostasis, challenges in the treatment of diabetes to Kennedy proposed that signals originated in avoid the development and progression of di- fat deposits would act at brain level, decreas- abetes complications1,2. ing appetite7. When various intestine pep- 75 Juan J. Gagliardino relation with age, insulin sensitivity, total HDL-cholesterol, HDL2 and HDL3. Patients with gastric bypass present low plasma ghre- lin levels, accounting for decreased appetite13. Ghrelin stimulates the secretion of soma- totrophin, ACTH, cortisol and prolactin14. Its effect upon insulin and glucagon varies as a function of the dose used: a low dose inhibits insulin secretion and stimulates glucagon se- cretion in vitro, whereas high doses stimulate insulin secretion without modifying glucagon secretion15. However, given the circulating levels of ghrelin, it would not exert a modula- tory physiological effect in vivo of the secre- tion of these hormones15. Figure 1.Integration of glycemic and energy homeosta- Ghrelin metabolic effects are opposite to sis. Combination of signals and effectors of two systems participating in the regulation of glycemic and energy those of leptin: it stimulates food intake, po- homeostasis. tentiates carbohydrate utilization, reduces fat utilization, increases gastric motility and stomach acid secretion, and would act as an tides and their receptors at the central ner- adipocity signal favoring weight gain12. These vous system (CNS) were identified, it was results suggest that both the effects and the postulated that their release in response to secretion of ghrelin are opposite to those of food intake generated “immediate” satiety leptin. signals at brain level, determining the inter- ruption of food intake8. The model was com- Oxyntomodulin (OXM) pleted when leptin was identified as a long- Oxyntomodulin is a 37 aminoacid peptide term adipocyte signal released in relation to resulting from the processing of proglucagon the size of body fat deposits; together with in- (Figure 2) in intestine L cells16, which inhibits sulin, leptin acts directly at the CNS, inhibit- the secretion of oxyntic glands in the ing food intake9. stomach17. To facilitate the understanding of post- OXM is released in the postprandial peri- prandial glycemic regulation and energy od by distal intestine endocrine cells that pro- homeostasis, we will first describe the signals duce peptides such as PYY18 and GLP-119, and mechanisms involved, then the regulato- and its circulating levels remain elevated for ry center, and finally how both models act. several hours after food intake20. OXM levels are markedly high in people with morbid Ghrelin obesity and jejuno-ileal bypass21 and are asso- Ghrelin is a 28 aminoacid lipophilic pep- ciated with nervous anorexy and weight tide with a labile octanoic acid side chain at loss22. Since OXM inhibits appetite at hypo- the serine residue, mainly expressed in ente- thalamic level, it would be part of a negative rochromaffin cells of the gastric mucosa10. feedback mechanism. Ghrelin has also been identified in pancreatic OXM binds to GLP-1 receptor, but with non-β islet cells11. It would circulate in plasma lower affinity23. In rats, however, the inhibito- bound to HDL-cholesterol particles, with de- ry effect of OXM on appetite is reduced by creased concentration peaks after food in- blocking GLP-1R receptors24. take, together with increased levels of in- OXM infusion for 90 min reduces the calo- sulin12. rie content of food (-20%); this effect lasts Ghrelin levels are low in positive energy for 12 h (-11%), without modifying signifi- balance conditions; they increase in people cantly calorie intake in the 24 h-period25. on a diet and have a negative correlation with OXM also decreases significantly the concen- fasting insulinemia, body weight, body mass tration of plasma ghrelin (appetite-stimulat- index (BMI), and adipocyte volume12. On the ing) before food intake, being such inhibition other hand, ghrelin levels have a positive cor- one of OXM´s satiety mechanisms. 76 Physiological endocrine control of energy homeostasis and postprandial blood glucose levels Figure 2. Proglucagon and processing systems. Different processing of proglucagon molecule in islet α-cells and in- testine L-cells. Numbers and letters indicate peptidase cleavage sites. OXM would act in the arcuate nucleus ry presynaptic receptor highly expressed in (AN) of the hypothalamus, where energy NPY neurons of the AN. homeostasis signals are monitored and inte- Intraperitoneal injection of PYY3-36 inhibits grated24. It would also act at in the vagus the daily food intake in a dose-dependent nerve, transmitting afferent signals to the manner acting on Y2 receptors, as demon- brain via ghrelin26. strated by its inactivity in mice with KO of that receptor. Peptide YY (PYY) In man, PYY perfusion in amounts capable This is a gastrointestinal peptide of 36 of reproducing the levels obtained in the aminoacids mainly produced by intestinal L postprandial period, reduce appetite and cells27 which belongs to the pancreatic food intake by 33% for 24 h, and decrease polypeptide family together with neuropep- significantly fasting and preprandial ghrelin 28 28 tide Y (NPY) . PYY becomes PYY3-36 levels . Such prolongued effect suggests that, through the action of dipeptidyl peptidase IV opposed to other intestinal peptides, PYY3-36 (DPP IV); circulating levels increase by 33% is a long-term appetite regulator31. 15 min after food intake and keep elevated In the AN, PYY3-36 would diminish the for approximately 90 min. The peak of PYY GABAergic tone through which NPY in- is proportional to the amount of calorie in- hibits proopiomelanocortin (POMC) neu- take; PYY decreases appetite and conse- rons, allowing the expression of their in- quently food intake through a negative feed- hibitory effect upon appetite32. back mechanism28,29. The early release of There is a negative correlation between PYY (15 min) is initially produced by nerve PYY levels and BMI, so that basal and post- stimulation and then as a function of the in- prandial PYY levels are lower in obese peo- testine nutrient content. ple. Since PYY is
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