Comparison between Parkinson's disease patients with body weight loss and those with body weight gain

Nicotine induces weight loss in both humans and rodents consuming a regular diet; however, the effect of nicotine on body weight and fat composition in rodents consuming a high-fat diet (HFD) has not been well studied. Thus, this study examined the effect of nicotine vs saline on body weight and fat composition in mice fed with either an HFD (62% of kcal from fat) or a standard normal chow diet (NCD) for 7 weeks. Nicotine dose dependently reduced body weight gain in mice that consumed both diets, but this effect was significantly greater in mice on the HFD. Caloric intake was decreased in nicotine-treated mice. Estimates of energy intake suggested that decreased caloric intake accounted for all the reduced weight gain in mice on an NCD and 66% of the reduced weight gain on an HFD. Computed tomography analysis for fat distribution demonstrated that nicotine was effective in reducing abdominal fat in mice that consumed the HFD, with nicotine treatment leading to lower visceral fat. The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the α4β2 nAChR partial agonist/antagonist, varenicline. We conclude that nicotine is effective in preventing HFD-induced weight gain and abdominal fat accumulation.

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The pathogenic effects of Eimeria praecox and E. acervulina in the chicken

Parasitology ◽

10.1017/s0031182000028997 ◽

1968 ◽

Vol 58 (3) ◽

pp. 691-700 ◽

Cited By ~ 30

Author(s):

P. L. Long

Keyword(s):

Weight Loss ◽

Body Weight ◽

Weight Gain ◽

Food Consumption ◽

Intestinal Permeability ◽

Technical Assistance ◽

Body Weight Gain ◽

Eimeria Acervulina ◽

No Weight Loss ◽

Pathogenic Effects

Eimeria praecox produced less effect on body-weight gain and food consumption than E. acervulina. No deaths occurred and no weight loss followed infection with doses of oocysts up to 10. However, there was a depression of body-weight gain in birds infected with both species and changes in the permeability of the intestine were noted from as early as 3½ h after infection. This suggests that increased intestinal permeability is not the major factor in the greater pathogenicity of E. acervulina compared with E. praecox. Eimeria acervulina produced considerably greater effects on the host as evidenced by mortality, body weight gain and food consumption.I wish to thank Mr B. J. Millard and Mr M. Shirley for technical assistance and Dr B. M. Freeman for help with the statistics in Table 2.

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Body weight gain rather than body weight variability associated with increased risk of nonalcoholic fatty liver disease

Scientific Reports ◽

10.1038/s41598-021-93883-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Eun Ju Cho ◽

Su Jong Yu ◽

Gu Cheol Jung ◽

Min-Sun Kwak ◽

Jong In Yang ◽

...

Keyword(s):

Weight Loss ◽

Body Weight ◽

Liver Disease ◽

Weight Gain ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Fatty Liver Disease ◽

Body Weight Gain ◽

Nonalcoholic Fatty Liver ◽

Increased Risk

AbstractWeight loss, the most established therapy for nonalcoholic fatty liver disease (NAFLD), is frequently followed by weight regain and fluctuation. The aim of this study was to investigate whether body weight change and variability were independent risk factors for incident NAFLD. We conducted a longitudinal cohort study. Among the 1907 participants, incident NAFLD occurred in 420 (22.0%) cases during median follow-up of 5.6 years. In the multivariate analysis, there was no significant association between weight variability and the risk of incident NAFLD. The risk of incident NAFLD was significantly higher in subjects with weight gain ≥ 10% and 7% < gain ≤ 10% [hazard ratios (HR), 2.43; 95% confidence intervals (CI), 1.65–3.58 and HR, 1.73; 95% CI, 1.26–2.39, respectively], while the risk of incident NAFLD was significantly lower in those with −7% < weight loss ≤ -−3% (HR, 0.33; 95% CI, 0.22–0.51). Overall body weight gain rather than bodyweight variability was independently associated with the risk of incident NAFLD. Understanding the association between body weight variability and incident NAFLD may have future clinical implications for the quantification of weight loss as a treatment for patients with NAFLD.

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Abstract 19336: Chronic Vagal Nerve Stimulation Causes Weight Loss by Reducing Food Intake and Feeding Efficiency in Mice

Circulation ◽

10.1161/circ.130.suppl_2.19336 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Harald M Stauss ◽

Daniel P Dias ◽

Donald A Morgan ◽

Kamal Rahmouni

Keyword(s):

Weight Loss ◽

Body Weight ◽

Oxygen Consumption ◽

Weight Gain ◽

Food Intake ◽

Metabolic Rate ◽

Body Weight Gain ◽

Caloric Intake ◽

Vagal Nerve ◽

Feeding Efficiency

Chronic electrical vagal nerve stimulation (VNS) has emerged as a new tool to treat human diseases including obesity. Indeed, chronic VNS has been shown to cause weight loss in humans and in experimental animal models. However, the mechanisms for VNS-induced weight loss are largely unknown. We hypothesized that an increase in metabolic rate together with reduced caloric intake and reduced feeding efficiency (body weight gain per calories consumed) contribute to chronic VNS-induced weight loss or reduced weight gain. To test this hypothesis, we developed a miniaturized microprocessor-operated nerve stimulator for chronic use in conscious mice. Effectiveness of the stimulator was verified by bradycardia at stimulation frequencies above 5 Hz (3V, 1mA, 1ms pulses). Male C57Bl/6 mice (16 weeks old, standard mouse chow diet) were instrumented with nerve stimulators (3V, 1mA, 1ms pulses at 5 Hz) on the right cervical vagal nerve and body weight, food intake and metabolic rate (indirect calorimetry) were determined at baseline and weekly thereafter. After the initial post-surgical weight loss, sham animals (n=9, stimulators off) regained pre-surgical body weight within 16 days (100.0±2.7%). In contrast, mice with chronic VNS (n=12) never reestablished pre-surgical body weight (94.5±0.9% on day 16, P<0.05 vs. sham). Caloric intake was significantly reduced in mice with chronic VNS compared to sham animals (74.7±2.4 vs. 84.6±4.2 kcal/week, P<0.05). Likewise, mice with chronic VNS showed significantly reduced feeding efficiency compared to sham mice (2.6±2.0 vs. 10.6±2.4 mg body weight gain per kcal consumed). Oxygen consumption tended to be elevated (2734±152 vs. 2490±124 mL/kg/h, P=0.23) during the first week, but not thereafter. In conclusion reduced food intake and lower feeding efficiency contribute to reduced weight gain in mice with chronic VNS. We speculate that an initial increase in metabolic rate (assessed by oxygen consumption) may be antagonized by compensatory mechanisms in response to chronic VNS.

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Orexin A-induced activity is inversely correlated with body weight gain and may promote weight loss in rats

Appetite ◽

10.1016/j.appet.2008.04.173 ◽

2008 ◽

Vol 51 (2) ◽

pp. 388

Author(s):

J.P. Nixon ◽

J.A. Teske ◽

C.J. Billington ◽

C.M. Kotz

Keyword(s):

Weight Loss ◽

Body Weight ◽

Weight Gain ◽

Body Weight Gain ◽

Orexin A ◽

Promote Weight Loss

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Effect of suckling intensity of primiparous sows on production performance during current and subsequent parities1

Journal of Animal Science ◽

10.1093/jas/skz341 ◽

2019 ◽

Vol 97 (12) ◽

pp. 4845-4854

Author(s):

Ji Yao Guo ◽

Yawang Sun ◽

Ashley E DeDecker ◽

Max Terry Coffey ◽

Sung Woo Kim

Keyword(s):

Weight Loss ◽

Body Weight ◽

Weight Gain ◽

Litter Size ◽

Removal Rate ◽

Body Weight Loss ◽

Production Performance ◽

Body Lipid ◽

Litter Weight ◽

Lactation Length

Abstract This study was conducted to evaluate the effects of suckling intensity (litter size and lactation length) to primiparious sows on production performance during current and subsequent parities. Upon farrowing, 115 primiparous sows (farrowing weight: 222.7 ± 20.0 kg) were initially allotted to 4 treatments in a 2 × 2 factorial arrangement with 2 litter sizes: 10 and 13 piglets (LS10 vs. LS13), and 2 lactation lengths: 21 and 27 d (LL21 vs. LL27). Upon weaning, sows were rebred and those farrowed successfully (n = 66) kept 10 piglets and weaned at 21 d in the second parity. Sows were fed ad libitum during lactation in both parities. Feed intake, BW loss, backfat loss, litter size, and litter weight gain during lactation in both parities were determined. Litter weight gain in LS13 was greater (P < 0.05) than that in LS10 (54.4 vs. 47.7 kg) during the first lactation. Sows in LS13 had a greater (P < 0.05) BW loss than sows in LS10 (24.1 vs. 17.4 kg). Body weight loss was not different between LL27 and LL21. Sows in LS13 tended to have a greater (P = 0.075) removal rate than those in LS10 (47.5 vs. 32.2%). Sows in LL27 had a smaller (P < 0.05) removal rate than those in LL21 (28.0 vs. 51.7%). In the second parity, gestation BW gain in LL27 tended to be greater (P = 0.098) than that in LL21 when the previous litter size was 10 piglets (56.1 vs. 33.2 kg). Litter performance and feed intake of sows were not affected by previous litter size, lactation length, and their interaction. The farrowing weight, farrowing body protein and lipid, body weight loss was not different between LS13 and LS10, whereas backfat loss in LS13 was smaller (P < 0.05) than that in LS10 during the second lactation (0.9 vs. 2.4 mm). The predicted body lipid loss in LS13 was also smaller than that in LS10 (2.3 vs. 5.3 kg) during the second lactation. Sows in LL27 had a smaller (P < 0.05) BW loss and body lipid loss during the second lactation than sows in LL21 (4.0 vs. 9.0 kg; 2.3 vs. 4.8 kg). The concentration of milk fat in LL27 was smaller (P < 0.05) than that in LL21 (7.9 vs. 9.1%). In conclusion, increasing suckling intensity to primiparous sows increased litter weight gain but increasing litter size reduced piglet ADG. Sow performance in the second lactation was not negatively affected by increasing suckling intensity of the first lactation. Interestingly, sows with an increased suckling intensity in the first lactation had reduced loss of body reserves in the second lactation.

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Responses of Adipose and Muscle Lipoprotein Lipase to Chronic Infection and Subsequent Acute Lipopolysaccharide Challenge

Clinical and Vaccine Immunology ◽

10.1128/cdli.9.4.771-776.2002 ◽

2002 ◽

Vol 9 (4) ◽

pp. 771-776 ◽

Cited By ~ 1

Author(s):

Frédéric Picard ◽

Denis Arsenijevic ◽

Denis Richard ◽

Yves Deshaies

Keyword(s):

Weight Loss ◽

Body Weight ◽

Weight Gain ◽

Energy Balance ◽

Lipoprotein Lipase ◽

Neospora Caninum ◽

Body Weight Gain ◽

Acute Response ◽

Lps Treatment

ABSTRACT Infection of male Swiss Webster mice with Toxoplasma gondii or Neospora caninum leads to long-term alterations in energy balance. Following an initial 20 to 30% weight loss in all T. gondii-infected mice, half of the animals regain most of the lost weight (gainers), whereas the others maintain their low body weight (nongainers). Infection with N. caninum does not elicit weight loss. Lipoprotein lipase (LPL), the enzyme responsible for plasma triglyceride (TG) clearance and partitioning among tissues, is under tissue-specific modulation associated with energy balance. It is also a major determinant of infection-induced hypertriglyceridemia. This study aimed to assess the long-term modulation of adipose and muscle LPL activity in mice infected with T. gondii or N. caninum, to evaluate the effects of subsequent acute lipopolysaccharide (LPS) administration, and to relate LPL modulation in these conditions with infection-related changes in body weight gain. Twenty-eight days after infection, LPL activity in muscle of both gainer and nongainer T. gondii-infected mice was reduced by 40 to 50% compared with the levels in controls and N. caninum-infected mice, whereas LPL activity in adipose depots remained unchanged in all infected groups compared to the level in controls. LPS (from Escherichia coli, 100 ng/kg) injection induced a global reduction in adipose LPL in all groups, as assessed 90 min later. In both T. gondii-infected subgroups, muscle LPL was not further reduced by LPS treatment, whereas it was decreased by 40 to 50% in muscles of control and N. caninum-infected mice. Pre-LPS TG levels in plasma were similar in all groups. LPS greatly increased TG levels in plasma in both control and N. caninum-infected animals, whereas it did not alter those of T. gondii-infected gainer or nongainer animals. These results show that (i) independently of the extent of postinfection weight gain, long-term infection with T. gondii chronically reduces muscle LPL, which becomes unresponsive to acute endotoxemia; (ii) modulation of tissue LPL activity during chronic T. gondii infection favors TG partitioning towards adipose tissue; and (iii) skeletal muscle LPL is a key determinant of the acute response of triglyceridemia to LPS.

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