The scourge of obesity arising from obesogens and poor dieting still ravages our planet as half of the global population may be overweight and obese by 2035. This metabolic disorder is intertwined with type 2 diabetes (T2D), both of which warrant alternative therapeutic options other than clinically approved drugs like orlistat with their tendency of abuse and side effects. In this review, we comprehensively describe the global obesity problem and its connection to T2D. Obesity, overconsumption of fats, the mechanism of fat digestion, obesogenic gut microbiota, inhibition of fat digestion, and natural anti-obesity compounds are discussed. Similar discussions are made for diabetes with regard to glucose regulation, the diabetic gut microbiota, and insulinotropic compounds. The sources and production of anti-obesity bioactive peptides (AOBPs) and anti-diabetic bioactive peptides (ADBPs) are also described while explaining their structure–function relationships, gastrointestinal behaviors, and action mechanisms. Finally, the techno-functional applications of AOBPs and ADBPs are highlighted. 

Anti-obesity and anti-diabetic bioactive peptides: A comprehensive review of their sources, properties, and techno-functional challenges.

To investigate the therapeutic effects and mechanisms of Semaglutide in Alzheimer's disease (AD), and identify its potential targets. 

Semaglutide ameliorates Alzheimer's disease and restores oxytocin in APP/PS1 mice and human brain organoid models

The hypothalamic neuropeptide and hormone oxytocin are of fundamental importance for maternal, social, and sexual behavior. Deviations in oxytocin levels have also been associated with anxiety, autism spectrum disorders (ASD), depression, ADHD (attention deficit hyperactivity disorder), and schizophrenia. Both oxytocin and dopamine are often considered reward- and feel-good hormones, and dopamine is associated with the above-mentioned behaviors and, and dopamine is also associated with the above-mentioned behaviors and disorders. Although being structurally totally different, oxytocin, a peptide, and dopamine, a monoamine, they have a number of similar effects. They are synthesized both in the brain and in the periphery, and they affect each other’s release and receptors. In addition, oxytocin and dopamine are released in response to, for example, social interaction, sex, feeding, and massage. This review discusses interactions between oxytocin and dopamine with a specific focus on behavioral effects and possible roles of oxytocin and dopamine in various mental disorders and functional diversities. 

Interactions of Oxytocin and Dopamine—Effects on Behavior in Health and Disease

Growing evidence suggests that oxytocin (OT) plays an important factor for the control of food intake, body weight, and energy metabolism in human and non-human animals. It has reported previously, the downregulation in oxytocin receptors (OTRs) expression is linked with the development of obesity, but exogenous OT reverse body weight and food intake in obese animal model. It is important to know that, whether intraperitoneal administration crosses blood brain barrier. Therefore, in the present experiment, we study the impact of intraperitoneal administration of synthetic OT 0.0116 mg/kg and antagonist atosiban (OTA) 1 mg/kg on food intake, and body weight of female mice, Mus musculus for different duration i.e. 30, 60, and 90 days. In this study, it was observed that there was significant decrease (p<0.001, one-way analysis of variance [ANOVA]) in the body weight (BW), food intake, and gonadosmatic indices (GSI) after the intraperitoneal exposure of OT at dose 0.0116 mg/kg up to 90 days and inhibits via antagonist atosiban. These results indicates that intraperitoneal administration of OT can be used for treatment for longer duration without any side effects and maintains homeostasis in physiologic system regulates body weight and gonadal weight in female mice, which represent an important therapeutic tool for the obesity and metabolic disorder in female.

Effects of oxytocin and antagonist antidote atosiban on body weight and food intake of female mice, Mus musculus.

INTRODUCTION
GLP-1 receptor agonists are the number one drug prescribed for the treatment of obesity and type 2 diabetes. These drugs are not, however, without side-effects and in an effort to maximize therapeutic effect while minimizing adverse effects, gut hormone co-agonists received considerable attention as new drug targets in the fight against obesity. Numerous previous reports identified the neuropeptide oxytocin (OXT) as a promising anti-obesity drug. The aim of this study is to evaluate OXT as a possible co-agonist for GLP-1 and examine the effects of its co-administration on food intake (FI) and body weight (BW) in mice.


METHODS
FI and c-Fos levels were measured in the feeding-centers of the brain in response to an intraperitoneal injection of saline, OXT, GLP-1 or OXT/GLP-1. The action potential frequency and cytosolic Ca2+ ([Ca2+]i) in response to OXT, GLP-1 or OXT/GLP-1were measured in ex-vivo PVN neuronal cultures. Finally, FI and BW changes were compared in diet induced obese mice treated with saline, OXT, GLP-1 or OXT/GLP-1 for 13 days.


RESULTS
Single injection of OXT/GLP-1 additively decreased FI, and increased c-Fos expression specifically in the paraventricular (PVN) and supraoptic nucleus (SON). 70% of GLP-1 receptor positive neurons in the PVN also expressed OXT receptors, and OXT/GLP-1 co-administration dramatically increased firing and [Ca2+]i in the PVN OXT neurons. The chronic OXT/GLP-1 co-administration decreased BW without changing FI.


CONCLUSION
Chronic OXT/GLP-1 co-administration decreases BW, possibly via the activation of PVN OXT neurons. OXT might be a promising candidate as an incretin co-agonist in obesity treatment.

Systemic co-administration of low dose oxytocin and glucagon like peptide-1 additively decreases food intake and body weight.

Antagonistic interaction between central glucagon-like Peptide-1 and oxytocin on diet-induced obesity mice.

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Antagonistic interaction between central glucagon-like Peptide-1 and oxytocin on diet-induced obesity mice.