Experimental obesity and osteoarthritis

1960 ◽  
Vol 198 (4) ◽  
pp. 765-770 ◽  
Author(s):  
Leon Sokoloff ◽  
Olaf Mickelsen ◽  
Emanuel Silverstein ◽  
George E. Jay ◽  
Richard S. Yamamoto
Keyword(s):  
Weight Gain ◽  
Dietary Restriction ◽  
High Fat Diet ◽  
Deleterious Effect ◽  
Degenerative Joint Disease ◽  
Fat Content ◽  
Joint Disease ◽  
High Fat ◽  
Low Fat ◽  
Hybrid Mice

Experimental obesity was produced in DBA/2JN, STR/N and C57L/HeN mice as well as in Osborne-Mendel rats by several dietary regimens. One of these, containing 60% vegetable fat, increased the amount of degenerative joint disease in the rats and in two strains of mice. No increase of osteoarthritis occurred as a result of a 37.4% fat content in the diet, or from obesity produced by Ingle's diet, which has a relatively low-fat content. The mechanism by which the high-fat diet increased the joint disease is unknown, because neither obesity nor a high-fat diet alone had a deleterious effect on the articulations of the mice. Obese hybrid mice derived from a spontaneously obese and arthritis-prone strain (STR/1N) were resistant to articular degeneration. Dietary restriction of weight gain in the STR/1N mice failed to decrease the osteoarthritis in them.

scholarly journals High-fat and low-fat (behavioural) phenotypes: biology or environment?

1999 ◽  
Vol 58 (4) ◽  
pp. 773-777 ◽  
Author(s):  
John E. Blundell ◽  
John Cooling
Keyword(s):  
Risk Factors ◽  
Body Weight ◽  
Risk Factor ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Positive Energy ◽  
High Fat ◽  
Low Fat ◽  
Conceptual Tool

It is now widely accepted that obesity develops by way of genetic mechanisms conferring specific dispositions which interact with strong environmental pressures. It is also accepted that certain dispositions constitute metabolic risk factors for weight gain. It is less well accepted that certain patterns of behaviour (arising from biological demands or environmental influences) put individuals at risk of developing a positive energy balance and weight gain (behavioural risk factors). Relevant patterns of behaviour include long-lasting habits for selecting and eating particular types of foods. Such habits define two distinct groups characterized as high-fat (HF) and low-fat (LF) phenotypes. These habits are important because of the attention given to dietary macronutrients in body-weight gain and the worldwide epidemic of obesity. Considerable evidence indicates that the total amount of dietary fat consumed remains the most potent food-related risk factor for weight gain. However, although habitual intake of a high-fat diet is a behavioural risk factor for obesity, it does not constitute a biological inevitability. A habitual low-fat diet does seem to protect against the development of obesity, but a high-fat diet does not guarantee that an individual will be obese. Although obesity is much more prevalent among HF than LF, some HF are lean with BMI well within the normal range. The concept of 'different routes to obesity' through a variety of nutritional scenarios can be envisaged, with predisposed individuals varying in their susceptibility to different dietary inputs. In a particular subgroup of individuals (young adult males) HF and LF displayed quite different profiles of appetite control, response to nutrient challenges and physiological measures, including BMR, RQ, heart rate, plasma leptin levels and thermogenic responses to fat and carbohydrate meals. These striking differences suggest that HF and LF can be used as a conceptual tool to investigate the relationship between biology and the environment (diet) in the control of body weight.

scholarly journals Macronutrient balances and obesity: the role of diet and physical activity

1999 ◽  
Vol 2 (3a) ◽  
pp. 341-347 ◽  
Author(s):  
Arne Astrup
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Physical Fitness ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Oxidation ◽  
Fat Content ◽  
High Fat

AbstractObservational cross-sectional and longitudinal studies suggest that a high fat diet and physical inactivity are independent risk factors for weight gain and obesity. Mechanistic and intervention studies support that fat possesses a lower satiating power than carbohydrate and protein, and a diet low in fat therefore decreases energy intake. The effect of dietary fat on energy balance is enhanced in susceptible subjects, particularly in sedentary individuals with a genetic predisposition to obesity who consume a high fat diet.Dietary carbohydrate promotes its own oxidation by an insulin-mediated stimulation of glucose oxidation. In contrast, high fat meals do not increase fat oxidation acutely. A sedentary life-style and low physical fitness cause a low muscular fat oxidation capacity, and the consumption of a high fat diet by these individuals promotes fat storage in a synergistic fashion.Ad libitum low fat diets cause weight loss proportional to pre-treatment body weight in a dose-dependent way, i.e. weight loss is correlated positively to the reduction in dietary fat content. Increased physical activity prevents relapse after weight loss and studies have shown that those who keep up a higher level of physical activity are more successful in maintaining the reduced body weight. In conclusion, important interactions exist between genetic make up, dietary fat and physical fitness, so that a low fitness level and susceptible genes reduce muscular fat oxidation capacity which may decrease the tolerance of dietary fat. Increasing daily physical activity and reducing dietary fat content may be more effective when combined than when separate in preventing weight gain and obesity.

scholarly journals Systemic versus local adipokine expression differs in a combined obesity and osteoarthritis mouse model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marie-Lisa Hülser ◽  
Yubin Luo ◽  
Klaus Frommer ◽  
Rebecca Hasseli ◽  
Kernt Köhler ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Medial Meniscus ◽  
Degenerative Joint Disease ◽  
Mechanisms Of Action ◽  
Normal Diet ◽  
Joint Disease ◽  
Metabolic Effects ◽  
High Fat ◽  
Joint Function ◽  
Diet Induced Obesity

AbstractOsteoarthritis (OA) is a degenerative joint disease characterized by cartilage loss and reduced joint function. OA risk factors are age and obesity. Many adipokines are altered by obesity but also OA although systemic adipokine regulation in OA is not always clear. Therefore, metabolic effects of diet-induced obesity on OA development as well as the influence of obesity and OA progression on systemic vs. local adipokine expression in joints were compared. C57Bl/6-mice fed with HFD (high fat diet) or normal diet prior to destabilization of the medial meniscus (DMM) were sacrificed 4/6/8 weeks after surgery. Sera were evaluated for adiponectin, leptin, visfatin, cytokines. Liver grading and staging for non-alcoholic steatohepatitis (NASH) was performed and crown-like structures (CLS) in adipose tissue measured. OA progression was scored histologically. Adipokine-expressing cells and types were evaluated by immunohistochemistry. Time-dependent changes in DMM-progression were reflected by increased systemic adiponectin levels in DMM especially combined with HFD. While HFD increased serum leptin, DMM reduced systemic leptin significantly. OA scores correlated with bodyweight, leptin and hepatic scoring. Locally, increased numbers of adiponectin- and leptin-producing fibroblasts were observed in damaged menisci but visfatin was not changed. Local adipokine expression was independent from systemic levels, suggesting different mechanisms of action.

scholarly journals Increased expression of receptors for orexigenic factors in nodose ganglion of diet-induced obese rats

2009 ◽  
Vol 296 (4) ◽  
pp. E898-E903 ◽  
Author(s):  
Gabriel Paulino ◽  
Claire Barbier de la Serre ◽  
Trina A. Knotts ◽  
Pieter J. Oort ◽  
John W. Newman ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Afferent Pathway ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Vagal Afferent

The vagal afferent pathway is important in short-term regulation of food intake, and decreased activation of this neural pathway with long-term ingestion of a high-fat diet may contribute to hyperphagic weight gain. We tested the hypothesis that expression of genes encoding receptors for orexigenic factors in vagal afferent neurons are increased by long-term ingestion of a high-fat diet, thus supporting orexigenic signals from the gut. Obesity-prone (DIO-P) rats fed a high-fat diet showed increased body weight and hyperleptinemia compared with low-fat diet-fed controls and high-fat diet-induced obesity-resistant (DIO-R) rats. Expression of the type I cannabinoid receptor and growth hormone secretagogue receptor 1a in the nodose ganglia was increased in DIO-P compared with low-fat diet-fed controls or DIO-R rats. Shifts in the balance between orexigenic and anorexigenic signals within the vagal afferent pathway may influence food intake and body weight gain induced by high fat diets.

scholarly journals Dietary fat and corticosterone levels are contributing factors to meal anticipation

2016 ◽  
Vol 310 (8) ◽  
pp. R711-R723 ◽  
Author(s):  
Sara Namvar ◽  
Amy Gyte ◽  
Mark Denn ◽  
Brendan Leighton ◽  
Hugh D. Piggins
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Content ◽  
High Fat ◽  
Contributing Factors ◽  
Low Fat ◽  
Restricted Access ◽  
Fos Expression ◽  
Fat Feeding

Daily restricted access to food leads to the development of food anticipatory activity and metabolism, which depends upon an as yet unidentified food-entrainable oscillator(s). A premeal anticipatory peak in circulating hormones, including corticosterone is also elicited by daily restricted feeding. High-fat feeding is associated with elevated levels of corticosterone with disrupted circadian rhythms and a failure to develop robust meal anticipation. It is not clear whether the disrupted corticosterone rhythm, resulting from high-fat feeding contributes to attenuated meal anticipation in high-fat fed rats. Our aim was to better characterize meal anticipation in rats fed a low- or high-fat diet, and to better understand the role of corticosterone in this process. To this end, we utilized behavioral observations, hypothalamic c-Fos expression, and indirect calorimetry to assess meal entrainment. We also used the glucocorticoid receptor antagonist, RU486, to dissect out the role of corticosterone in meal anticipation in rats given daily access to a meal with different fat content. Restricted access to a low-fat diet led to robust meal anticipation, as well as entrainment of hypothalamic c-Fos expression, metabolism, and circulating corticosterone. These measures were significantly attenuated in response to a high-fat diet, and animals on this diet exhibited a postanticipatory rise in corticosterone. Interestingly, antagonism of glucocorticoid activity using RU486 attenuated meal anticipation in low-fat fed rats, but promoted meal anticipation in high-fat-fed rats. These findings suggest an important role for corticosterone in the regulation of meal anticipation in a manner dependent upon dietary fat content.

Daily consumption of monoglucosyl-rutin prevents high-fat diet-induced obesity by suppressing gastric inhibitory polypeptide secretion in mice

2018 ◽  
Vol 8 (7) ◽  
pp. 353 ◽  
Author(s):  
Daigo Yokoyama ◽  
Wataru Tanaka ◽  
Yushi Hashizume ◽  
Mahamadou Tandia ◽  
Masanobu Sakono ◽  
...  
Keyword(s):  
Weight Gain ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Gastric Inhibitory Polypeptide ◽  
Diet Group ◽  
Antioxidant Defenses ◽  
High Fat ◽  
Low Fat ◽  
Daily Consumption ◽  
Low Fat Diet

Background: Alpha monoglucosyl-rutin (4G-α-D-glucopyranosyl rutin, αMR) has been shown to stimulate antioxidant defenses and anti-glycation. We evaluated the effects of αMR on body weight gain in mice.Methods: Male C57BL/6J mice were divided into four groups: Control low-fat diet, low-fat diet + 0.5% αMR, high-fat diet, and high-fat diet + 0.5% αMR. Blood chemistry, hepatic lipids, and serum metabolic hormones and cytokines were evaluated after 4 and 13 weeks.Results: After 6 weeks, the high-fat diet group gained more weight than the low-fat diet group. Supplementing the high-fat diet with αMR suppressed weight gain by week 13. Visceral fat weight was higher in the high-fat diet group on weeks 4 and 13, while αMR supplementation inhibited increase on week 13 but not on week 4. Serum levels of gastric inhibitory polypeptide were higher in the high-fat-diet group than in the low-fat-diet group. αMR supplementation inhibited this elevation and regulated levels of serum leptin and hepatic triglycerides.Conclusion: For the first time, we demonstrated how daily consumption of αMR inhibits diet-induced visceral fat accumulation by regulating the secretion of gastric inhibitory polypeptide, which thereby prevents excess weight gain. Therefore, αMR may be a promising potential functional food.Keywords: Anti-obesity; gastric inhibitory polypeptide; mouse; alpha monoglucosyl-rutin; quercetin

Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

1994 ◽  
Vol 71 (06) ◽  
pp. 755-758 ◽  
Author(s):  
E M Bladbjerg ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen
Keyword(s):  
High Fat Diet ◽  
Fat Content ◽  
Factor Vii ◽  
Amidolytic Activity ◽  
High Fat ◽  
Low Fat Diet ◽  
Increased Risk ◽  
Coagulant Activity ◽  
High Fat Diets ◽  
Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

scholarly journals Berberine elevates cardiolipin in heart of offspring from mouse dams with high fat diet-induced gestational diabetes mellitus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura K. Cole ◽  
Genevieve C. Sparagna ◽  
Marilyne Vandel ◽  
Bo Xiang ◽  
Vernon W. Dolinsky ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Mitochondrial Function ◽  
High Fat Diet ◽  
Fatty Acid Uptake ◽  
Isoquinoline Alkaloid ◽  
Acid Uptake ◽  
High Fat ◽  
Low Fat

AbstractBerberine (BBR) is an isoquinoline alkaloid from plants known to improve cardiac mitochondrial function in gestational diabetes mellitus (GDM) offspring but the mechanism is poorly understood. We examined the role of the mitochondrial phospholipid cardiolipin (CL) in mediating this cardiac improvement. C57BL/6 female mice were fed either a Lean-inducing low-fat diet or a GDM-inducing high-fat diet for 6 weeks prior to breeding. Lean and GDM-exposed male offspring were randomly assigned a low-fat, high-fat, or high-fat diet containing BBR at weaning for 12 weeks. The content of CL was elevated in the heart of GDM offspring fed a high fat diet containing BBR. The increase in total cardiac CL was due to significant increases in the most abundant and functionally important CL species, tetralinoleoyl-CL and this correlated with an increase in the expression of the CL remodeling enzyme tafazzin. Additionally, BBR treatment increased expression of cardiac enzymes involved in fatty acid uptake and oxidation and electron transport chain subunits in high fat diet fed GDM offspring. Thus, dietary BBR protection from cardiac dysfunction in GDM exposed offspring involves improvement in mitochondrial function mediated through increased synthesis of CL.

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