scholarly journals Some biological aspects of partial starvation. The effect of weight loss and regrowth on body compsition in sheep

1974 ◽  
Vol 32 (3) ◽  
pp. 515-527 ◽  
Author(s):  
J. H. Burton ◽  
M. Anderson ◽  
J. T. Reid

1. A study of the effects of four dietary treatments on body-weight and the water, protein, fat and energy content of the empty bodies of forty-three Suffolk ewes is reported. The treatments were as follows: T1, ad lib. food intake from a full-body-weight (FBW) of 40 kg to 71 kg; T2, partial fasting with a resulting weight loss from 71 kg to 50 kg FBW; T3, realimentation and regrowth from 50 kg to 71 kg FBW; T4, a slight food restriction producing a reduced growth rate from 40 kg to 50 kg FBW followed by ad lib. food intake from 50 kg to 71 kg FBW. On all treatments sheep were slaughtered in groups of three at 7 kg intervals between 50 kg and 71 kg FBW.2. The whole body, with the exception of several body organs and glands, wool and the contents of the gastrointestinal tract, was minced and analysed for water, protein, fat and energy. Adipose tissue samples were removed at slaughter from subcutaneous and internal fat depots for histological examination. Regression analysis was used in comparing treatment effects on body composition.3. No significant differences were observed between the results of T1 and T4. In consequence these results were pooled and are referred to as T1. At 40 kg FBW the empty (ingesta-free) bodies of the lambs contained approximately 52% water, 14 % protein and 29% fat. Through normal growth to 71 kg FBW on T1 these values had changed to 40, 11.5 and 45 %, respectively. Following weight loss to 50 kg FBW on T2 the water, protein and fat contents of the empty bodies were 47, 13.5 and 35 %, respectively. Regrowth on T3 to 71 kg FBW resulted in little change in these components, the respective values being 46, 13 and 36 %. The sheep which had undergone weight loss and regrowth retained significantly more water and less energy than normally grown controls and tended to deposit less fat and more protein.4. Gastrointestinal tract contents accounted for 11 % of FBW at 71 kg in T3 animals. In T1, the value was 7.1 % at a similar FBW. Thus there was an average increase of over 56 % in contents in the realimented animals.5. Mean adipocyte diameter at 50 kg FBW on T1 was 134 ± 3 μm. At 71 kg FBW the mean diameter had increased to 152 ± 9 μm. Weight reduction (T2) and regrowth (T3) resulted in mean diameters of 122 ± 4 μm and 143 ± 4 μm at 50 kg and 71 kg FBW, respectively.

2017 ◽  
Vol 313 (1) ◽  
pp. E37-E47 ◽  
Author(s):  
Judith N. Gorski ◽  
Michele J. Pachanski ◽  
Joel Mane ◽  
Christopher W. Plummer ◽  
Sarah Souza ◽  
...  

G protein-coupled receptor 40 (GPR40) partial agonists lower glucose through the potentiation of glucose-stimulated insulin secretion, which is believed to provide significant glucose lowering without the weight gain or hypoglycemic risk associated with exogenous insulin or glucose-independent insulin secretagogues. The class of small-molecule GPR40 modulators, known as AgoPAMs (agonist also capable of acting as positive allosteric modulators), differentiate from partial agonists, binding to a distinct site and functioning as full agonists to stimulate the secretion of both insulin and glucagon-like peptide-1 (GLP-1). Here we show that GPR40 AgoPAMs significantly increase active GLP-1 levels and reduce acute and chronic food intake and body weight in diet-induced obese (DIO) mice. These effects of AgoPAM treatment on food intake are novel and required both GPR40 and GLP-1 receptor signaling pathways, as demonstrated in GPR40 and GLP-1 receptor-null mice. Furthermore, weight loss associated with GPR40 AgoPAMs was accompanied by a significant reduction in gastric motility in these DIO mice. Chronic treatment with a GPR40 AgoPAM, in combination with a dipeptidyl peptidase IV inhibitor, synergistically decreased food intake and body weight in the mouse. The effect of GPR40 AgoPAMs on GLP-1 secretion was recapitulated in lean, healthy rhesus macaque demonstrating that the putative mechanism mediating weight loss translates to higher species. Together, our data indicate effects of AgoPAMs that go beyond glucose lowering previously observed with GPR40 partial agonist treatment with additional potential for weight loss.


1982 ◽  
Vol 35 (2) ◽  
pp. 284-293 ◽  
Author(s):  
H S Koopmans ◽  
A Sclafani ◽  
C Fichtner ◽  
P F Aravich

2008 ◽  
Vol 18 (4) ◽  
pp. 415-422 ◽  
Author(s):  
Marianne W. Furnes ◽  
Karin Tømmerås ◽  
Carl-Jørgen Arum ◽  
Chun-Mei Zhao ◽  
Duan Chen

1998 ◽  
Vol 274 (6) ◽  
pp. R1518-R1525 ◽  
Author(s):  
Atsushi Kaibara ◽  
Armin Moshyedi ◽  
Troy Auffenberg ◽  
Amer Abouhamze ◽  
Edward M. Copeland ◽  
...  

The ob gene product leptin is known to produce anorexia and loss of body fat when chronically administered to both lean and genetically obese mice. The current study was undertaken to examine whether administration of recombinant leptin in quantities sufficient to produce decreases in food intake and body weight and alterations in body composition would elicit either an hepatic acute phase protein response or preferential loss of carcass lean tissue. Mice were administered increasing quantities of recombinant human leptin or human tumor necrosis factor-α as a positive control. Although leptin (at 10 mg/kg body wt) produced significant anorexia and weight loss (both P < 0.05), human leptin administration did not appear to induce an hepatic acute phase protein response in either lean or genetically obese mice, as determined by protein synthetic rates in the liver or changes in the plasma concentration of the murine acute phase protein reactants, amyloid A, amyloid P, or seromucoid (α1-acid glycoprotein). In addition, human leptin administration did not induce a loss of fat-free dry mass (protein) in lean or obese animals. The findings suggest that at doses adequate to alter food intake and body weight leptin is not a significant inducer of the hepatic acute phase response nor does leptin promote the preferential loss of somatic protein characteristic of a chronic inflammatory process.


2004 ◽  
Vol 91 (3) ◽  
pp. 479-484 ◽  
Author(s):  
Alejandro E. Macias

The existence of a set-point for homeostatic control of human body weight is uncertain. To investigate its existence, technically difficult determinations of energy expenditure must be performed: this has resulted in contradictory reports. The present study was performed with new methods in two stages (77 and 133d respectively). Two healthy male subjects with rigorously controlled physical activity ingested three standardized diets of processed foods from the same manufacturer. Hypo-, iso- and hyperenergetic diets containing 6255kJ (1494kcal), 10073kJ (2406kcal) and 13791kJ (3294kcal) respectively were ingested during alternate periods; changes in body weight were measured. A new index of energy expenditure was calculated as the amount of weight lost in an 8h overnight period (WL8H). A digital scale was used in stage 1 and a mechanical scale in stage 2. The change in body weight in response to the isoenergetic diet differed according to the circumstances. In basal conditions, it was associated with weight stability. After weight loss from energy restriction, the isoenergetic diet led to weight gain. After weight gain from overeating, it led to weight loss. Diets of higher energy content were associated with greater WL8H (F>20; P<0·0001 for both subjects). Measurement variability was lower using a mechanical scale. The present study demonstrates the existence of a homeostatic control of human weight and describes a new index of energy expenditure measured in weight units. It also demonstrates that strict dietary supervision for months is possible. Investigation of the human body weight set-point is vital in understanding obesity.


2020 ◽  
Vol 11 ◽  
Author(s):  
Do-Hyun Kim ◽  
Joong Sun Kim ◽  
Jeongsang Kim ◽  
Jong-Kil Jeong ◽  
Hong-Seok Son ◽  
...  

Licorice and dried ginger decoction (Gancao-ganjiang-tang, LGD) is used for nausea and anorexia, accompanied by excessive sweating in Traditional Chinese Medicine. Herein, we investigated the therapeutic effects of LGD using the activity-based anorexia (ABA) in a mouse model. Six-week-old female BALB/c AnNCrl mice were orally administered LGD, water, licorice decoction, dried ginger decoction, or chronic olanzapine, and their survival, body weight, food intake, and wheel activity were compared in ABA. Additionally, dopamine concentration in brain tissues was evaluated. LGD significantly reduced the number of ABA mice reaching the drop-out criterion of fatal body weight loss. However, LGD showed no significant effects on food intake and wheel activity. We found that in the LGD group the rise of the light phase activity rate inhibited body weight loss. Licorice or dried ginger alone did not improve survival rates, they only showed longer survival periods than chronic olanzapine when combined. In addition, LGD increased the dopamine concentration in the brain. The results from the present study showed that LGD improves the survival of ABA mice and its mechanism of action might be related to the alteration of dopamine concentration in the brain.


Author(s):  
Francesco Cavagnini

Appetite is regulated by a complex system of central and peripheral signals that interact in order to modulate eating behavior according the individual needs, i.e. the fasting or fed condition and the general nutritional status. Peripheral regulation includes adiposity signals and satiety signals, while central control is accomplished by several effectors, including the neuropeptidergic, monoaminergic and endocannabinoid systems. Adiposity signals inform the brain of the general nutritional status of the subject as indicated by the extent of fat depots. Indeed, leptin produced by the adipose tissue and insulin, whose pancreatic secretion tends to increase with the increase of fat mass, convey to the brain an anorexigenic message. Satiety signals, including cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), originate from the gastrointestinal tract during a meal and, through the vagus nerve, reach the nucleus tractus solitarius (NTS) in the caudal brainstem. From NTS afferents fibers project to the arcuate nucleus (ARC) of the hypothalamus, where satiety signals are integrated with adiposity signals and with several hypothalamic and supra-hypothalamic inputs, thus creating a complex network of neural circuits that finally elaborate the most appropriate response, in terms of eating behavior. In more detail, ARC neurons secrete a number of neuropeptides with orexigenic properties, such as neuropeptide Y (NPY) and agouti-related peptide (AGRP), or anorexigenic effects such as pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). Other brain areas involved in the control of food intake are located downstream the ARC: among these, the paraventricular nucleus (PVN), which produces anorexigenic peptides such as thyrotropin releasing hormone (TRH), corticotrophin releasing hormone (CRH) and oxytocin, the lateral hypothalamus (LHA) and perifornical area (PFA), secreting the orexigenic substances orexin-A (OXA) and melanin concentrating hormone (MCH). Recently, a great interest has developed for endogenous cannabinoids, important players in the regulation of food intake and energy metabolism. In the same context, increasing evidence is accumulating for a role played by the microbiota, the trillion of microorganism populating the human gastrointestinal tract. The complex interaction between the peripheral organs and the central nervous system has generated the concept of gut-brain axis, now incorporated into the physiology. A better understanding of the mechanisms governing the eating behavior will allow the development of drugs capable of reducing or enhancing food consumption.


Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 6054-6061 ◽  
Author(s):  
Jonathan D. Roth ◽  
Todd Coffey ◽  
Carolyn M. Jodka ◽  
Holly Maier ◽  
Jennifer R. Athanacio ◽  
...  

Circulating levels of the pancreatic β-cell peptide hormone amylin and the gut peptide PYY[3–36] increase after nutrient ingestion. Both have been implicated as short-term signals of meal termination with anorexigenic and weight-reducing effects. However, their combined effects are unknown. We report that the combination of amylin and PYY[3–36] elicited greater anorexigenic and weight-reducing effects than either peptide alone. In high-fat-fed rats, a single ip injection of amylin (10 μg/kg) plus PYY[3–36] (1000 μg/kg) reduced food intake for 24 h (P &lt; 0.05 vs. vehicle), whereas the anorexigenic effects of either PYY[3–36] or amylin alone began to diminish 6 h after injection. These anorexigenic effects were dissociable from changes in locomotor activity. Subcutaneous infusion of amylin plus PYY[3–36] for 14 d suppressed food intake and body weight to a greater extent than either agent alone in both rat and mouse diet-induced obesity (DIO) models (P &lt; 0.05). In DIO-prone rats, 24-h metabolic rate was maintained despite weight loss, and amylin plus PYY[3–36] (but not monotherapy) increased 24-h fat oxidation (P &lt; 0.05 vs. vehicle). Finally, a 4 × 3 factorial design was used to formally describe the interaction between amylin and PYY[3–36]. DIO-prone rats were treated with amylin (0, 4, 20, and 100 μg/kg·d) and PYY[3–36] (0, 200, 400 μg/kg·d) alone and in combination for 14 d. Statistical analyses revealed that food intake suppression with amylin plus PYY[3–36] treatment was synergistic, whereas body weight reduction was additive. Collectively, these observations highlight the importance of studying peptide hormones in combination and suggest that integrated neurohormonal approaches may hold promise as treatments for obesity.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 5166-5166
Author(s):  
Oktawiusz Wiecha ◽  
Witold Miezynski ◽  
Leszek Wojakiewicz ◽  
Anna Zebzda ◽  
Anna Wedrychowicz ◽  
...  

Abstract Graft versus host disease (GvHD) is still a very serious problem in hematopoietic stem cells transplantation which makes searching for new possibilities of its prevention and treatment necessary. Animal models are very useful tools for such research. We present a mouse model of GvHD allowing observation of both acute and chronic phase of the disease. C57Bl/6 mice (H-2b) were transplanted, one day after ablative TBI with 5×106 BM cells and 4×106 or 10×106 splenocytes isolated from allogeneic C3H. He (H-2k) or from syngeneic animals. Sex mismatched transplants were performed and chimerism of transplanted animals was confirmed by detection of sry gene with PCR. As a control group for blood examination after transplantation C3H syngeneic transplantations were performed. After transplantation, mice were weighted and physically examined by looking for changes in skin, posture, physical activity and peripheral blood parameters. Histopathological examination was performed on day +8, +16, +31 in some of the animals. Autopsy was also performed on mice which died during the experiment or which body weight decreased below 65% of the initial weight. We observed a characteristic pattern of physical symptoms of GvHD including weight loss, skin desquamation, hunching and loss of activity, diarrhea. Weight loss to 88.2% of the initial body weight on day +7 was followed by a return to the initial weight (101.1%) on day +14 and then another decrease either strong and leading to the death of the animal or moderate and leading to a long time plateau (the average body weight on days +31, +59 and +101 was 94.4%, 91.7% and 93.6%). On day +7 desquamation of the skin of paws was very well visible and since day +10 gradually intensifying desquamative changes of the skin of whole body were observed - the mean level of changes in the population was highest on days +21 to + 24. Interestingly areas of the skin which were nude before TBI and transplantation were affected earlier (changes were visible on day +7) and more severly than other regions of the skin suggesting that local more intensive damage caused by irradiation can locally aggravate the course of GvHD. The physical symptoms were accompanied with histopathological changes of liver, skin, spleen and gut. Neither physical nor histopathological symptoms of the disease were observed in mice transplanted with syngeneic cells. In fluorocytometric analysis of peripherial blood performed on days +17, +31 and +45 severe lymphopenia was observed. The average number of CD3+CD4+, CD3+CD8+ and B220+ cells was strongly decreased in animals transplanted with allogeneic cells as compared to syngeneic graft recipients. At the same time expression of CD69 activation antigen on CD4+ and CD8+ cells was strongly increased in allograft recipients as compared to syngeneic controls. The course of the disease, including weight loss and skin changes, was generally less severe in the population of mice transplanted with BM + 4×106 splenocytes as compared to BM + 10×106 of splenocytes recipients. The 25th, 50th and 75th percentiles of survival function for both populations were162, 301, 405 and 45, 88, 277 days, respectively.


2005 ◽  
Vol 90 (2) ◽  
pp. 820-825 ◽  
Author(s):  
Karen E. Foster-Schubert ◽  
Anne McTiernan ◽  
R. Scott Frayo ◽  
Robert S. Schwartz ◽  
Kumar B. Rajan ◽  
...  

Weight loss resulting from decreased caloric intake raises levels of the orexigenic hormone, ghrelin. Because ingested nutrients suppress ghrelin, increased ghrelin levels in hypophagic weight loss may result from decreased inhibitory input by ingested food, rather than from lost weight. We assessed whether ghrelin levels increase in response to exercise-induced weight loss without decreased caloric intake. We randomized 173 sedentary, overweight, postmenopausal women to an aerobic exercise intervention or stretching control group. At baseline, 3 months, and 12 months, we measured body weight and composition, food intake, cardiopulmonary fitness (maximal oxygen consumption), leptin, insulin, and ghrelin. Complete data were available for 168 women (97%) at 12 months. Exercisers lost 1.4 ± 0.4 kg (P &lt; 0.05 compared with baseline; P = 0.01 compared with stretchers) and manifested a significant, progressive increase in ghrelin levels, whereas neither measure changed among stretchers. Ghrelin increased 18% in exercisers who lost more than 3 kg (P &lt; 0.001). There was no change in caloric intake in either group and no effect on ghrelin of exercise per se independent of its impact on body weight. In summary, ghrelin levels increase with weight loss achieved without reduced food intake, consistent with a role for ghrelin in the adaptive response constraining weight loss and, thus, in long-term body weight regulation.


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