Although laparoscopic cholecystectomy rapidly became the standard of care for the surgical treatment of cholelithiasis, very few other abdominal or cardiac operations are currently performed using minimally invasive surgical techniques. The inherent limitations of traditional laparoscopic surgery make it difficult to perform these operations. We, and others, have attempted to use robotic technology to (a) provide a stable camera platform, (b) replace two-dimensional with three-dimensional (3-D) imaging, (c) simulate the fluid motions of a surgeon's wrist to overcome the motion limitations of straight laparoscopic instruments, and (d) offer the surgeon a comfortable, ergonomically optimal operating position. In this article, we review the early published clinical experience with surgical robotic and telerobotic systems and assess their current limitations. The voice-controlled AESOP robot replaces the cameraperson and facilitates the performance of solo-surgeon laparoscopic operations. AESOP provides a stable camera platform and avoids motion sickness in the operative team. The telerobotic Zeus and da Vinci surgical systems permit solo surgery by a surgeon from a remote sight. These telerobots hold the camera, replace the surgeon's two hands with robotic instruments, and serve in a master-slave relationship for the surgeon. Their robotic instruments simulate the motions of the surgeon's wrist, facilitating dissection. Both telerobots use 3-D imaging to immerse the surgeon in a three-dimensional video operating field. These robots also provide operating positions for the surgeon console that are ergonomically superior to those required by traditional laparoscopy. The technological advances of these telerobots now permit telepresence surgery from remote locations, even locations thousands of miles away. In addition, telepresence permits the telementoring of novice surgeons who are performing new procedures by expert surgeons in remote locations. The studies reviewed here indicate that robotics and telerobotics offer potential solutions to the inherent problems of traditional laparoscopic surgery, as well as new possibilities for telesurgery and telementoring. Nonetheless, these technologies are still in an early stage of development, and each device entails its own set of challenges and limitations for actual use in clinical settings.

Robotic-assisted laparoscopic low anterior resection for rectal cancer is feasible in experienced hands. This technique may facilitate minimally invasive radical rectal surgery.

Telerobotic-assisted laparoscopic colectomy is feasible and warrants further investigations in controlled trials.

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Peptide YY (PYY) is a 36 amino acid, straight chain polypeptide, which is co-localized with GLP-1 in the L-type endocrine cells of the GI mucosa. PYY shares structural homology with neuropeptide Y (NPY) and pancreatic polypeptide (PP), and together form the Neuropeptide Y Family of Peptides, which is also called the Pancreatic Polypeptide-Fold Family of Peptides. PYY release is stimulated by intraluminal nutrients, including glucose, bile salts, lipids, short-chain fatty acids and amino acids. Regulatory peptides such as cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), gastrin and GLP-1 modulate PYY release. The proximal GI tract may also participate in the regulation of PYY release through vagal fibers. After release, dipeptidyl peptidase IV (DPP-IV; CD 26) cleaves the N-terminal tyrosine-proline residues forming PYY(3-36). PYY(1-36) represents about 60% and PYY(3-36) 40% of circulating PYY. PYY acts through Y-receptor subtypes: Y1, Y2, Y4 and Y5 in humans. PYY(1-36) shows high affinity to all four receptors while PYY(3-36) is a specific Y2 agonist. PYY inhibits many GI functions, including gastric acid secretion, gastric emptying, small bowel and colonic chloride secretion, mouth to cecum transit time, pancreatic exocrine secretion and pancreatic insulin secretion. PYY also promotes postprandial naturesis and elevates systolic and diastolic blood pressure. PYY(1-36) and PYY(3-36) cross the blood-brain barrier and participate in appetite and weight control regulation. PYY(1-36) acting through Y1- and Y5-receptors increases appetite and stimulates weight gain. PYY(3-36) acting through Y2-receptors on NPY-containing cells in the arcuate nucleus inhibits NPY release and, thereby, decreases appetite and promotes weight loss. PYY may play a primary role in the appetite suppression and weight loss observed after bariatric operations.