Type 2 diabetes is a high-profile global public health problem, particularly in Asia. The young age of onset, low body mass index, and early appearance of pancreatic islet dysfunction are characteristics of Asian patients with T2DM. Metabolic surgery has become the standard treatment for T2DM patients and can significantly improve T2DM through a variety of mechanisms including modulation of energy homeostasis and reduction of body fat mass. Indeed, restoration of islet function also plays an integral role in the remission of T2DM. After metabolic surgery, islet function in Asian T2DM patients has improved significantly, with proven short-term and long-term effects. In addition, islet function is an important criterion and reference for patient selection prior to metabolic surgery. The mechanism of islet function improvement after metabolic surgery is not clear, but postoperative anatomical changes in the gastrointestinal tract leading to a number of hormonal changes seem to be the potential cause, including glucagon-like peptide-1, gastric inhibitory polypeptide, peptide YY, ghrelin, and cholecystokinin. The authors analyzed the current retrospective and prospective studies on the effect of metabolic surgery on the islet function of Asian T2DM patients with a low BMI and its mechanism, summarized the clinical evidence that metabolic surgery improved islet function in Asian T2DM patients with a low BMI, and discussed its underlying mechanism. It is of great significance for realizing personalized and precise treatment of metabolic surgery and further improving its clinical benefits.
Bariatric Surgery ; Body Mass Index ; Cholecystokinin/therapeutic use* ; Diabetes Mellitus, Type 2/surgery* ; Gastric Inhibitory Polypeptide/therapeutic use* ; Ghrelin/therapeutic use* ; Glucagon-Like Peptide 1/therapeutic use* ; Humans ; Peptide YY/therapeutic use* ; Prospective Studies ; Retrospective Studies ; Treatment Outcome

BACKGROUND: A premeal load of protein can increase satiety and reduce energy intake. Dietary fiber also conveys metabolic benefits by modulating energy intake. We made a protein-enriched, dietary fiber-fortified bar (PFB) and aimed to investigate its effects on food intake and gut hormone secretion in healthy individuals.METHODS: Twenty subjects with normal glucose tolerance were enrolled. On three separate visits, the subjects received, in a randomized order, one of the following: a PFB containing 73 kcal with 10.7 g of protein and 12.7 g of dietary fiber; a usual bar (UB) containing the same calories as the PFB but only 0.9 g of protein and no dietary fiber; or water (control). After 15 minutes, the subjects had ad libitum intake of a test meal. Food consumption, appetite, and plasma gut hormone levels were measured.RESULTS: Total energy intake, including the bar and the test meal, was significantly reduced with the PFB preload compared to the water (904.4±534.9 kcal vs. 1,075.0±508.0 kcal, P=0.016). With the UB preload, only the intake of the test meal was reduced (P=0.044) but not the total energy intake (P=0.471) than the water. Fullness was also significantly increased after the PFB. In addition, postprandial glucose levels decreased and glucagon-like peptide-1 levels increased with the PFB compared with both the UB and water.CONCLUSION: In healthy individuals, a premeal supplementation of PFB reduced total energy intake and decreased postprandial glucose excursion. This finding necessitates long-term studies regarding clinical use in obesity.
Appetite ; Dietary Fiber ; Eating ; Energy Intake ; Glucagon-Like Peptide 1 ; Glucose ; Meals ; Obesity ; Peptide YY ; Plasma ; Water

PURPOSE: The purpose of this study is to clarify the relevance of breastfeeding and its preventive effect on maternal hypertension as well as to evaluate the theoretical mechanism behind of it through systematic evaluation of existing articles. METHODS: For systematic evaluation of literatures in recent 5 years, 5 most suitable articles were selected with the key words, (breastfeeding or breastfeed or lactation) AND (hypertension or high blood pressure or hypertensive disorders) from PubMed, EMBASE, and Cochran Library, and carefully reviewed by 2 researchers. RESULTS: Breastfeeding women have less frequently developed hypertension in their later life. Depending on the duration of breastfeeding, compared to nonbreastfeeding women, breastfeeding women's odds ratio for developing hypertension are 0.87 (95% confidence interval [CI], 0.76–0.99), 0.83 (95% CI, 0.68–1.00), and 0.79 (95% CI, 0.65–0.97) each for 0–6 months, 6–12 months, and greater than 12 months of breastfeeding. As the number of breastfeeding children increases, the incidence of maternal hypertension decreases. In addition, both partial and exclusive breastfeeding lower the risk of developing maternal hypertension. Though the mechanism of prophylactic effect of breastfeeding on hypertension is not conclusive, reset hypothesis, oxytocin release, the increase of ghrelin and protein peptide YY, as well as epigenetic programming are considered to be relevant to the etiology of the condition. CONCLUSION: Breastfeeding prevents maternal hypertension later in life. Studies show dose-response relationship of breastfeeding as the duration matters. In addition, both partial and exclusive breastfeeding have preventive effect on maternal hypertension. Numerous mechanisms are continuously being reported and further studies are needed for clarification.
Breast Feeding ; Child ; Epigenomics ; Female ; Ghrelin ; Humans ; Hypertension ; Incidence ; Odds Ratio ; Oxytocin ; Peptide YY

Strumal carcinoid tumor of the ovary is a rare subtype of ovarian carcinoid tumors; it is characterized by an intimate mixture of thyroid and carcinoid tissues. We present a case of a 64-year-old woman who presented with the chief complaint of persistent, severe constipation for over 5 years; she was later found to have an ovarian strumal carcinoid tumor. Computed tomography showed a well-defined solid mass measuring 6.4 cm at the right adnexa. The patient underwent right salpingo-oophorectomy and was histopathologically diagnosed as having a strumal carcinoid tumor. Immunohistochemical examination showed immunoreactivity for peptide YY (PYY), which exerts an inhibitory effect on the peristaltic actions of the distal intestine. After surgery, the patient's constipation resolved rapidly, suggesting a correlation between PYY producing ovarian carcinoid tumor and constipation. This is the first case report of PYY producing primary strumal carcinoid tumor of the ovary associated with persistent, severe constipation from Korea.
Carcinoid Tumor* ; Constipation* ; Female ; Humans ; Intestines ; Korea ; Middle Aged ; Ovary* ; Peptide YY* ; Thyroid Gland

This review focuses on the control of appetite by food intake-regulatory peptides secreted from the gastrointestinal tract, namely cholecystokinin, glucagon-like peptide 1, peptide YY, ghrelin, and the recently discovered nesfatin-1 via the gut-brain axis. Additionally, we describe the impact of external factors such as intake of different nutrients or stress on the secretion of gastrointestinal peptides. Finally, we highlight possible conservative—physical activity and pharmacotherapy—treatment strategies for obesity as well as surgical techniques such as deep brain stimulation and bariatric surgery also altering these peptidergic pathways.
Appetite ; Bariatric Surgery ; Cholecystokinin ; Deep Brain Stimulation ; Eating* ; Gastrointestinal Tract ; Ghrelin ; Glucagon-Like Peptide 1 ; Obesity* ; Peptide YY ; Peptides*

Chronic diseases such as obesity and diabetes are major causes of death and disability throughout the world. Many causes are known to trigger these chronic diseases, and infectious agents such as viruses are also pathological factors. In particular, it is considered that adenovirus 36 infections may be associated with obesity. If this is the case, a vaccine against adenovirus 36 may be a form of prophylaxis to combat obesity. Other types of therapeutic vaccines to combat obesity are also being developed. Recently, hormones such as glucagon-like peptide-1, ghrelin, and peptide YY have been studied as treatments to prevent obesity. This review describes the ongoing development of therapeutic vaccines to treat obesity, and the possibility of using inactivated adenovirus 36 as a vaccine and an anti-obesity agent.
Adenoviridae ; Cause of Death ; Chronic Disease ; Ghrelin ; Glucagon-Like Peptide 1 ; Obesity* ; Peptide YY ; Vaccines*

The prevalence of obesity has been rapidly increasing worldwide over the last several decades and has become a major health problem in developed countries. The brain, especially the hypothalamus, plays a key role in the control of food intake by sensing metabolic signals from peripheral organs and modulating feeding behaviors. To accomplish these important roles, the hypothalamus communicates with other brain areas such as the brainstem and reward-related limbic pathways. The adipocyte-derived hormone leptin and pancreatic beta-cell-derived insulin inform adiposity to the hypothalamus. Gut hormones such as cholecystokinin, peptide YY, pancreatic polypeptide, glucagon-like peptide 1, and oxyntomodulin transfer satiety signals to the brain and ghrelin relays hunger signals. The endocannabinoid system and nutrients are also involved in the physiological regulation of food intake. In this article, we briefly review physiological mechanisms of appetite regulation.
Adiposity ; Appetite ; Appetite Regulation ; Brain ; Brain Stem ; Cholecystokinin ; Developed Countries ; Eating ; Endocannabinoids ; Feeding Behavior ; Ghrelin ; Glucagon-Like Peptide 1 ; Hunger ; Hypothalamus ; Insulin ; Leptin ; Obesity ; Oxyntomodulin ; Pancreatic Polypeptide ; Peptide YY ; Prevalence

Understanding the relationship between energy nutrients compositions in a diet and appetite-controlling substances is essential for providing sound advice to anyone attempting to control body weight. Appetite is known to be affected by various hormones, ghrelin and peptide tyrosine-tyrosine (PYY), which are related to the compositions of a diet. The purpose of this study was to investigate the effects of compositions of energy nutrients in the diet on the levels of postprandial appetite-related hormones and satiety in healthy adult women. Ten subjects (BMI: 18.5-22.9 kg/m2) were recruited and assigned to three iso-coloric breakfast meals with different compositions of energy nutrients, regular meal (RM, CHO: 60%, Pro: 20%, Fat: 20%), high protein meal (HPM, CHO: 30%, Pro: 50%, Fat: 20%), and high fat meal (HFM, CHO: 30%, Pro: 20%, Fat: 50%). Blood levels of ghrelin, PYY, insulin and leptin and satiety were assessed at baseline, 30, 60, 90, 120, and 180 min following the consumption of each meal. There was no significant difference in the fasting blood hormones among the subjects taking each meals at baseline. Blood levels of ghrelin and insulin changed significantly following the consumption of each meal (p<0.05) over time, however no significant difference was shown between experimental meals until 180 min. Blood levels of PYY and leptin were not changed following the ingestion of each meals. In conclusion, the composition of energy nutrients in a diet had no effect on the postprandial plasma levels of ghrelin, PYY, insulin and leptin as well as satiety in healthy adult women.
Adult ; Appetite ; Body Weight ; Breakfast ; Diet ; Eating ; Fasting ; Female* ; Ghrelin ; Humans ; Insulin ; Leptin ; Meals ; Peptide YY ; Plasma ; Satiation

BACKGROUND/AIMS: It is generally believed that cholecystokinin (CCK) stimulates colonic motility, although there are controversial reports. It has also been suggested that postprandial peptide YY (PYY) release is CCK-dependent. Using a totally isolated, vascularly perfused rat colon, we investigated: (1) the roles of CCK and PYY on colonic motility, (2) to determine if CCK modulates PYY release from the colon to influence the motility and (3) to clarify whether the action of CCK and PYY on colonic motility is mediated via the influence of cholinergic input. METHODS: An isolated whole rat colon was used. Luminal pressure was monitored via microtip catheter pressure transducers from proximal and distal colon. After a control period, CCK-8 or PYY was administerd intraarterially with or without an anti-PYY serum, loxiglumide or atropine at 12, 60 and 240 pM. Each dose was given for a period of 15-minute and the contractile response was expressed as % changes over basal. PYY concentration in the portal effluent was determined by radioimmunoassay. RESULTS: Exogenous CCK-8 increased colonic motility which paralleled the increase in PYY release in the portal effluent. Exogenous PYY also significantly increased colonic motility although it was less potent than CCK. The stimulating effect of CCK-8 was significantly inhibited by an anti-PYY serum, and was completely abolished by loxiglumide, and almost completely abolished by atropine. CONCLUSIONS: CCK increases colonic motility via CCK1 receptor and it is mediated partly by PYY. Cholinergic input is required for the increased motility by either PYY or CCK.
Animals ; Atropine ; Catheters ; Cholecystokinin ; Colon ; Peptide YY ; Phenobarbital ; Proglumide ; Rats ; Sincalide ; Transducers, Pressure

PURPOSE: Obesity is considered an epidemic worldwide. Nonsurgical treatment such as dietary, physical and pharmacological therapies have limited success and thus, bariatric surgery is the ultimate option. Roux-en-Y gastric bypass (RYGB) is a bariatric procedure, which is a restrictive and malabsorptive procedure simultaneously. The purpose of this study was to develop surgical rat models of bariatric surgery and analyze the effect of gastric bypass on body weight, ghrelin and polypeptide YY(3-36) (PYY(3-36)) changes in rats. METHODS: RYGB, sleeve gastrectomy (SG) and sham operation were performed in diet-induced obese rats and compared to obese control and normal control rats. RESULTS: In RYGB group, 20.7+/-8.56% of weight loss was achieved on postoperative day 18 and maintained thereafter. This outcome was significant compared to SG (8.8+/-1.82%) and sham operated (6.2+/-2.45%) groups. When pre- and postoperative ghrelin levels were compared, there was a significant decrease in RYGB group (P<0.028); nonetheless, there was no difference in SG and sham operated groups. When pre- and postoperative PYY(3-36) levels were compared, there was a significant increase in RYGB (P<0.028), SG (P<0.031) and sham operated (P<0.031) groups. CONCLUSION: We developed surgical rat models of RYGB and SG. Those rats that underwent RYGB lost significant body weight and maintained the weight thereafter. The decrease in ghrelin and increase in PYY(3-36) may be associated with loss of appetite and delay in intestinal transit time with subsequent weight loss maintenance. In the future, this rat model would serve as a tool for further study on endocrine regulation of obesity.
Animals ; Appetite ; Bariatric Surgery ; Body Weight ; Gastrectomy ; Gastric Bypass ; Ghrelin ; Models, Animal ; Obesity ; Peptide YY ; Rats ; Salicylamides ; Weight Loss