Page 426 - Small Animal Clinical Nutrition 5th Edition
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440        Small Animal Clinical Nutrition




                    Box 25-1. Regulation of Food Intake.
        VetBooks.ir  For many years it has been known that the hypothalamus is the  thermogenesis. Obese patients appear to be leptin resistant, which


                    center of appetite control. Although voluntary food intake can vary  may impede their ability to regulate body weight.
                    in amount and composition from day to day, over time, energy  Gut peptides (ghrelin, PYY, GLP-1, PP, oxm) and hormones
                    intake is matched to energy expenditure. Body weight is tightly con-  (insulin and leptin) act directly on the arcuate nucleus of the hypo-
                    served; therefore, food intake, meal frequency and size are highly  thalamus. The arcuate nucleus has two populations of neurons. The
                    regulated. The role of peripheral and central pathways involved in  orexigenic neurons release two neuropeptides, neuropeptide  Y
                    appetite control is being studied as obesity increases in human and  (NPY) and agouti-related peptide (AgRP), which stimulate feeding
                    pet populations.                                 and promote obesity. The anorexigenic neuron center acts as an
                     Appetite is the desire for food and is often used synonymously  appetite inhibitor with the neuropeptides alpha-MSH and cocaine
                    with hunger. Satiety is the opposite of hunger and means that  and amphetamine-regulated transcript (CART).
                    hunger has been satisfied.The body is normally in a state of hunger,  These neuron centers of the arcuate nucleus project to the par-
                    which is intermittently relieved by eating. Hunger and satiety cen-  aventricular nucleus of the hypothalamus. The paraventricular
                    ters are found in the brain. The lateral hypothalamus contains the  nucleus receives direct input from other peripheral signals.
                    hunger center; stimulation of this area causes an animal to eat  Peripheral CCK, nutrients, vagal and sensory spinal signals travel to
                    voraciously. The ventromedial hypothalamus contains the satiety  the NTS, which then acts directly on the paraventricular nucleus.
                    center. Stimulation of this area causes complete satiety. Many neu-  Central signals to the paraventricular nucleus include the
                    roendocrine and metabolic factors affect these centers and there-  appetite stimulator, melanin-concentrating hormone (MCH) of the
                    fore contribute to appetite control.             lateral hypothalamus. The cortex and limbic system integrate
                     Short- and long-term input from the periphery including nutri-  appetite signals with the paraventricular nucleus. The paraventricu-
                    ents, gut vagal nerves, sensory spinal nerves, gut peptides and gut  lar nucleus then coordinates both central and peripheral signaling
                    hormones act on the arcuate nucleus of the hypothalamus. The  for feeding, energy metabolism, sympathetic nervous system activ-
                    peptide, ghrelin, released from the stomach, is the “hormone of  ity and the endocrine axis.
                    hunger.” Ghrelin is released in response to gut nutrients rather than  In addition, the special senses of taste and smell are involved in
                    gastric distention. Peptide YY (PYY) is an appetite depressant. It  the regulation of food intake. Taste is mediated through taste buds
                    affects gut motility centrally, acting as an “ileal brake.” Neural con-  and free nerve endings. Taste bud cells are constantly renewed by
                    trol of PYY is demonstrated by its release shortly after food intake  dividing epithelial cells surrounding the taste buds. Taste buds are
                    before nutrients reach the small intestine and colon, the site of  located on the tongue, soft palate, pharynx, larynx, epiglottis, cra-
                    highest PYY concentrations. Glucagon like peptide-1 (GLP-1) acts  nial esophagus and even on the lips and cheeks of some species.
                    on the pancreas to cause release of insulin and inhibit food intake.  Gustatory information received from taste buds is projected by cra-
                    Its rapid enzymatic breakdown has limited its potential use in Type  nial nerves to several areas of the brain including the lateral hypo-
                    II diabetics. Other gut peptides, pancreatic peptide (PP) and oxynto-  thalamus. Olfaction occurs via axons of bipolar neurons that course
                    modulin (oxm) play roles in decreasing food intake and homeostat-  through the small holes of the cribriform plate of the ethmoid bone
                    ic regulation of body weight. The peripheral appetite depressant,  and form connections in the olfactory bulb. As with taste, there are
                    cholecystokinin (CCK) is secreted in the duodenum in response to  olfactory projections to the hypothalamus.
                    fat and protein ingestion. CCK, gut vagal nerves and sensory spinal
                    nerves travel to the nucleus tractus solitarius (NTS) satiety center in  Donna Raditic, DVM
                    the brainstem.                                                 Angell Animal Medical Center
                     Insulin, released peripherally in proportion to body fat mass and  Boston, MA, USA
                    blood glucose levels, acts directly on hypothalamic appetite centers.
                    Another gut hormone, leptin, is released from adipocytes in direct  The Bibliography for Box 25-1 can be found at
                    relationship to body fat. Leptin decreases appetite and increases  www.markmorris.org.





                  synthesized more than twice the amount of globulin (12 g) than  Tissue Synthesis and Repair
                  those dogs fed the electrolyte solution (5.3 g) (Moss, 1978).  Tissue synthesis and wound healing are a function of local
                  Other cell populations and specific cell functions are likewise  and whole body nutritional status (Crane, 1989). On the cel-
                  quickly responsive to daily nutrient intake. Cats fed 25% of their  lular level, amino acids and carbohydrates are needed for col-
                  resting energy requirement (RER) for seven days had signifi-  lagen and ground substance synthesis. Fibroblasts require
                  cantly decreased total white blood cell (WBC) count, lympho-  energy to synthesize the RNA, DNA and ATP necessary for
                  cytes and monocytes;major histocompatibility complex (MHC)  protein anabolism. Migration of fibroblasts and epithelial and
                  class II expression; phagocytic activity; lymphocyte proliferative  endothelial cells also requires energy. On the organ level, the
                  capacity and delayed-type hypersensitivity response by Day 4.  liver has energy and protein needs specifically for synthesis of
                  These alterations were reversed by Day 4 of refeeding to meet  fibronectin, complement and glucose. The bone marrow
                  RER (Freitag et al, 2000; Simon et al, 2000). The immune sys-  requires nutrients for production of platelets, red blood cells
                  tem depends on and is responsive to adequate nutrition.  (RBC) and leukocytes. Transportation of these necessary
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