Appetite control: hormones or diet strategies?

PURPOSE OF REVIEW: Appetite control results from metabolic, behavioral, and environmental factors that influence hunger and the desire to eat. We summarize the latest advances in the hormonal and nutritional strategies to control appetite and reduce hunger. RECENT FINDINGS: The fed-hunger-state is regulated by central and peripheric hormones, which modulate energy balance. Leptin, insulin, ghrelin, peptide YY (PYY), and other gut-derived peptides represent the main appetite controllers. The role of orexins, obestatin, and liver-expressed antimicrobial peptide 2 has been uncovered recently. New insights have demonstrated the role of hippocampal activity as a possible mechanism of action. Glucagon-like peptide 1 (GLP1) receptor agonists are well known agents controlling appetite. Association of GLP1 receptor agonist, PYY, or glucose-dependent insulinotropic polypeptide agonists have been tested as new approaches. Appetite-control hormones have also risen as factors involved in the efficacy of bariatric procedures. High-protein, ketogenic diet, and intermittent fasting have been described as nutritional strategies to reduce appetite, although the physiological mechanism and long-term safety remains unclear. SUMMARY: Appetite control has been an important target for the treatment of obesity and associated disorders. New studies have demonstrated promising adoption of dietary approaches, hormone-based drugs, and bariatric surgery to control energy intake. Further research will establish a significant association, benefits, and safety of these new therapies.

Helminth infection modulates number and function of adipose tissue Tregs in high fat diet-induced obesity.

BACKGROUND: Epidemiological and experimental studies have shown a protective effect of helminth infections in weight gain and against the development of metabolic dysfunctions in the host. However, the mechanisms Treg cells exert in the helminth-obesity interface has been poorly investigated. The present study aimed to verify the influence of Heligmosomoides polygyrus infection in early stages of high fat diet-induced obesity. PRINCIPAL FINDINGS: The presence of infection was able to prevent exacerbated weight gain in mice fed with high fat diet when compared to non-infected controls. In addition, infected animals displayed improved insulin sensitivity and decreased fat accumulation in the liver. Obesity-associated inflammation was reduced in the presence of infection, demonstrated by lower levels of leptin and resistin, lower infiltration of Th1 and Th17 cells in adipose tissue, higher expression of IL10 and adiponectin, increased infiltration of Th2 and eosinophils in adipose tissue of infected animals. Of note, the parasite infection was associated with increased Treg frequency in adipose tissue which showed higher expression of cell surface markers of function and activation, like LAP and CD134. The infection could also increase adipose Treg suppressor function in animals on high fat diet. CONCLUSION: These data suggest that H. polygyrus modulates adipose tissue Treg cells with implication for weight gain and metabolic syndrome.

Inconsistent effects of gluten on obesity: is there a role for the haptoglobin isoforms?

BACKGROUND AND AIMS: There is no clear evidence about the effects of gluten intake on obesity. It is known that gluten's effects on gut permeability are mediated by zonulin, a protein identified as pre-haptoglobin 2, a physiological regulator of the intestinal barrier. We investigated the obesogenic and inflammatory effects of gluten and its association with the haptoglobin genotype. METHODS: This was a single blinded, crossover study, including 40 overweight or obesity women free of celiac disease. Participants adopted a gluten-free diet (GFD) for 8 weeks and consumed a gluten-free muffin (GF-M) or a gluten-containing muffin (GLU-M, 24 g gluten) for 4 weeks, switching muffin type during the subsequent 4 weeks. During a follow-up period of 4 weeks we evaluated the usual diet (UD). Food diaries were collected to estimate the macronutrient intake and dietary inflammatory index (DII®). Bodyweight and composition, resting energy expenditure (REE), and cytokines were assessed. Haptoglobin alleles (Hp1 and Hp2) were genotyped to characterize zonulin expression. RESULTS: Energy and macronutrient intakes were similar during both periods, except for protein intake, which was higher during GLU-M. DII scores indicated a more inflammatory profile during the GF-M and GLU-M periods compared to UD. No differences were observed in body composition or REE between interventions when the Hp genotype was not considered. Nonetheless, those carrying the Hp2-2 genotype (overexpressing zonulin) presented lower REE and higher levels of IL6 and IL1beta only during gluten intake (GLU-M and UD) compared to age- and body mass index-matched Hp1-1 carrier. These results suggest an obesogenic and inflammatory action of gluten only in those overexpressing zonulin (Hp2-2). CONCLUSION: These results highlight the importance of zonulin as the mediator of gluten obesogenic and inflammatory effects. Our data suggest that in the presence of gluten, zonulin release is associated with a reduction of REE and an increase of inflammatory markers that are not seen in zonulin low producers.