scholarly journals The ketogenic diet: a co-therapy in the treatment of mood disorders and obesity - a case report

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Agata Pieklik ◽  
Martyna Pawlaczyk ◽  
Joanna Rog ◽  
Hanna Karakuła-Juchnowicz
Keyword(s):  
Body Weight ◽  
Ketogenic Diet ◽  
Therapeutic Potential ◽  
Primary Source ◽  
Nutritional Intervention ◽  
Elevated Concentration ◽  
Body Weight Reduction ◽  
Reduced Body ◽  
The Central Nervous System

Abstract Introduction: There has been a growing interest in the ketogenic diet (KD) due to its suggested therapeutic potential to support numerous chronic diseases. KD is characterized by high amounts of fats and a reduced amount of carbohydrates and protein intake. During following the nutrition protocol, ketones are synthesised, which are the primary source of energy. The elevated concentration of ketones in blood serum inhibits hunger, what leads to reduced body weight. Some authors suggest KD has antidepressant potential and could stabilise mood by affecting neurotransmitters homeostasis in the central nervous system. Material and methods: The aim of the study was to assess the effect of KD on body weight reduction and improvement of mood in the patients with mood disorder diagnosis. To interpret the results of nutritional intervention, the laboratory parameters and structuralised scales and questionnaires were used. Results: After following 4-week therapy, the reduction of body weight, correction of some laboratory measurements and reduction in mood symptoms were noticed. Conclusions: The ketogenic diet affects the anthropometric measurements. However, a variety of simultaneous therapeutic approaches makes impossible determination of the effect on depressive symptoms.

scholarly journals Antagonism of central melanin-concentrating hormone 1 receptor alleviates steatohepatitis in mice

2008 ◽  
Vol 198 (2) ◽  
pp. 309-315 ◽  
Author(s):  
Makoto Ito ◽  
Akira Gomori ◽  
Jun Suzuki ◽  
Shigeharu Tsujioka ◽  
Minoru Sasaki ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Cytochromes P450 ◽  
Gene Expressions ◽  
Deficient Diet ◽  
Body Weight Reduction ◽  
Reduced Body ◽  
Intracerebroventricular Infusion ◽  
Melanin Concentrating Hormone

Blockade of brain melanin-concentrating hormone 1 receptor (MCH1R) significantly ameliorates fatty liver as well as obesity. However, the mode of action of this effect is unknown. This study examined the effect of a MCH1R antagonist in murine steatohepatitis models with and without obesity and clarified whether these pharmacological effects were attributed to anti-obesity effects. Steatohepatitis with concomitant obese phenotypes was developed after 52-week exposure to a high-fat diet, and steatohepatitis with reduced body weight was developed by exposure to a methionine- and choline-deficient diet for 10 days. Chronic intracerebroventricular infusion of a peptidic MCH1R antagonist reduced hepatic triglyceride contents and ameliorated steatohepatitis on histological observations in both mice models. Improvement of steatohepatitis was concomitant with amelioration of obese phenotypes such as hyperinsulinemia and hyperleptinemia in the case of the obese model, whereas body weight reduction was not associated with amelioration of steatohepatitis by the antagonist in the lean model. Reduction of hepatic gene expressions encoding cytochromes P450 4A was identified by treatment with the antagonist in both the obese and lean models. These results suggest that brain blockade of MCH1R could alleviate steatohepatitis independently from anti-obesity effects. In conclusion, MCH1R antagonist could have a new therapeutic potential for the treatment of human nonalcoholic steatohepatitis.

Determination of muscle activity during running at reduced body weight

2011 ◽  
Vol 29 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Jaco Liebenberg ◽  
Jennifer Scharf ◽  
Dana Forrest ◽  
Janet S. Dufek ◽  
K. Masumoto ◽  
...  
Keyword(s):  
Body Weight ◽  
Muscle Activity ◽  
Reduced Body

scholarly journals Effects of ambient temperature on adaptive thermogenesis during maintenance of reduced body weight in mice

2012 ◽  
Vol 303 (4) ◽  
pp. R438-R448 ◽  
Author(s):  
Yann Ravussin ◽  
Charles A. LeDuc ◽  
Kazuhisa Watanabe ◽  
Rudolph L. Leibel
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Ambient Temperature ◽  
Total Energy ◽  
Weight Reduction ◽  
Total Energy Expenditure ◽  
Fat Free Mass ◽  
Body Weight Reduction ◽  
Reduced Body ◽  
Basal Energy Expenditure

We showed previously that, at ambient room temperature (22°C), mice maintained at 20% below their initial body weight by calorie restriction expend energy at a rate below that which can be accounted for by the decrease of fat and fat-free mass. Food-restricted rodents may become torpid at subthermoneutral temperatures, a possible confounding factor when using mice as human models in obesity research. We examined the bioenergetic, hormonal, and behavioral responses to maintenance of a 20% body weight reduction in singly housed C57BL/6J +/+ and Lep ob mice housed at both 22°C and 30°C. Weight-reduced high-fat-fed diet mice (HFD-WR) showed similar quantitative reductions in energy expenditure—adjusted for body mass and composition—at both 22°C and 30°C: −1.4 kcal/24 h and −1.6 kcal/24 h below predicted, respectively, and neither group entered torpor. In contrast, weight-reduced Lep ob mice (OB-WR) housed at 22°C became torpid in the late lights-off period (0200–0500) but did not when housed at 30°C. These studies indicate that mice with an intact leptin axis display similar decreases in “absolute” energy expenditure in response to weight reduction at both 22°C and 30°C ambient temperature. More importantly, the “percent” decrease in total energy expenditure observed in the HFD-WR compared with AL mice is much greater at 30°C (−19%) than at 22°C (−10%). Basal energy expenditure demands are ∼45% lower in mice housed at 30°C vs. 22°C, since the mice housed at thermoneutrality do not allocate extra energy for heat production. The higher total energy expenditure of mice housed at 22°C due to these increased thermogenic demands may mask physiologically relevant changes in energy expenditure showing that ambient temperature must be carefully considered when quantifying energy metabolism in both rodents and humans.

scholarly journals Adipose tissue transplantation protects ob/ob mice from obesity, normalizes insulin sensitivity and restores fertility

2005 ◽  
Vol 186 (1) ◽  
pp. 203-211 ◽  
Author(s):  
Simon Klebanov ◽  
Clinton M Astle ◽  
Olga DeSimone ◽  
Vitaly Ablamunits ◽  
David E Harrison
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Therapeutic Potential ◽  
Body Weight Gain ◽  
Hormone Replacement ◽  
Tolerance Test ◽  
Reduced Body ◽  
Insulin Tolerance

Adipose tissue affects metabolism by secreting various adipokines. Lipodystropic mice benefit both from leptin replacement therapy and from transplantation of normal fat. Leptin-deficient Lepob/Lepob (ob/ob) mice can also be treated with leptin. Surprisingly, there have been no reports of successful treatment of obese ob/ob mice by transplantation of normal white adipose tissue (WAT). If WAT transplantation is ineffective in treating insulin resistance and diabetes in obese individuals, its applicability may be limited in humans as such abnormalities are usually associated with obesity. In the current study, we tested whether WAT transplantation might prevent, and even reverse, abnormalities characteristic of ob/ob mice. To assess the preventive potential, 6-week-old ob/ob mice were transplanted, subcutaneously, with gonadal fat pads from normal mice. Profound effects on multiple physiological phenotypes were achieved despite leptin levels below 25% of those in control mice. WAT from one donor reduced body weight gain, and WAT from 4 or 8 donors prevented obesity in ob/ob mice. Nonfasting insulin levels and insulin tolerance test were normalized. Corticosterone elevation was also prevented. Finally, WAT from 4 donors restored fertility in ob/ob females. The effects of WAT transplantation were long-lasting, with body weight gain suppressed for at least 40 weeks. To assess the therapeutic potential, obese 13-month-old ob/ob mice with a long history of leptin deficiency were used. Their body weight decreased by approximately 50% when transplanted with WAT from 8 donors. As in young recipients, transplantation greatly reduced nonfasting insulin, suggesting normalized insulin sensitivity. Thus, WAT transplantation was effective for both prevention and therapy. In the future, WAT transplantation may become a useful alternative to hormone replacement in treating not only lipodystropy, but also certain types of obesity.

Molecular and Phenotypic Analysis of Attractin Mutant Mice

Genetics ◽  
2001 ◽  
Vol 158 (4) ◽  
pp. 1683-1695 ◽  
Author(s):  
T M Gunn ◽  
T Inui ◽  
K Kitada ◽  
S Ito ◽  
K Wakamatsu ◽  
...  
Keyword(s):  
Body Weight ◽  
Mutant Mice ◽  
Compound Heterozygous ◽  
Phenotypic Analysis ◽  
Central Process ◽  
Molecular Abnormalities ◽  
Reduced Body ◽  
Pigment Type ◽  
The Central Nervous System ◽  
Relationship Of

Abstract Mutations of the mouse Attractin (Atrn; formerly mahogany) gene were originally recognized because they suppress Agouti pigment type switching. More recently, effects independent of Agouti have been recognized: mice homozygous for the Atrnmg-3J allele are resistant to diet-induced obesity and also develop abnormal myelination and vacuolation in the central nervous system. To better understand the pathophysiology and relationship of these pleiotropic effects, we further characterized the molecular abnormalities responsible for two additional Atrn alleles, Atrnmg and Atrnmg-L, and examined in parallel the phenotypes of homozygous and compound heterozygous animals. We find that the three alleles have similar effects on pigmentation and neurodegeneration, with a relative severity of Atrnmg-3J > Atrnmg > Atrnmg-L, which also corresponds to the effects of the three alleles on levels of normal Atrn mRNA. Animals homozygous for Atrnmg-3J or Atrnmg, but not Atrnmg-L, show reduced body weight, reduced adiposity, and increased locomotor activity, all in the presence of normal food intake. These results confirm that the mechanism responsible for the neuropathological alteration is a loss—rather than gain—of function, indicate that abnormal body weight in Atrn mutant mice is caused by a central process leading to increased energy expenditure, and demonstrate that pigmentation is more sensitive to levels of Atrn mRNA than are nonpigmentary phenotypes.

scholarly journals High Prevalence and Magnitude of Rapid Weight Loss in Mixed Martial Arts Athletes

2019 ◽  
Vol 29 (5) ◽  
pp. 512-517 ◽  
Author(s):  
Mathew Hillier ◽  
Louise Sutton ◽  
Lewis James ◽  
Dara Mojtahedi ◽  
Nicola Keay ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Martial Arts ◽  
Primary Source ◽  
Well Being ◽  
Rapid Weight Loss ◽  
Mixed Martial Arts ◽  
Reduced Body ◽  
Validated Questionnaire ◽  
High Prevalence

The practice of rapid weight loss (RWL) in mixed martial arts (MMA) is an increasing concern but data remain scarce. The aim of this study was to investigate the prevalence, magnitude, methods, and influencers of RWL in professional and amateur MMA athletes. MMA athletes (N = 314; 287 men and 27 women) across nine weight categories (strawweight to heavyweight), completed a validated questionnaire adapted for this sport. Sex-specific data were analyzed, and subgroup comparisons were made between athletes competing at professional and amateur levels. Most athletes purposefully reduced body weight for competition (men: 97.2%; women: 100%). The magnitude of RWL in 1 week prior to weigh-in was significantly greater for professional athletes compared with those competing at amateur level (men: 5.9% vs. 4.2%; women: 5.0% vs. 2.1% of body weight; p < .05). In the 24 hr preceding weigh-in, the magnitude of RWL was greater at professional than amateur level in men (3.7% vs. 2.5% of body weight; p < .05). Most athletes “always” or “sometimes” used water loading (72.9%), restricting fluid intake (71.3%), and sweat suits (55.4%) for RWL. Coaches were cited as the primary source of influence on RWL practices (men: 29.3%; women: 48.1%). There is a high reported prevalence of RWL in MMA, at professional and amateur levels. Our findings, constituting the largest inquiry to date, call for urgent action from MMA organizations to safeguard the health and well-being of athletes competing in this sport.

Mechanisms of Amylin/Leptin Synergy in Rodent Models

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 143-152 ◽  
Author(s):  
Victoria F. Turek ◽  
James L. Trevaskis ◽  
Barry E. Levin ◽  
Ambrose A. Dunn-Meynell ◽  
Boman Irani ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Leptin Receptor ◽  
Therapeutic Potential ◽  
Ventromedial Hypothalamus ◽  
Signal Transducer ◽  
Leptin Signaling ◽  
Reduced Body ◽  
Epididymal Fat ◽  
Transcription 3

Abstract The present studies aimed to identify mechanisms contributing to amylin/leptin synergy in reducing body weight and adiposity. We reasoned that if amylin/leptin harnessed complementary neuronal pathways, then in the leptin-sensitive state, amylin should augment leptin signaling/binding and that in the absence of endogenous amylin, leptin signaling should be diminished. Amylin (50 μg/kg, ip) amplified low-dose leptin-stimulated (15 μg/kg, ip) phosphorylated signal transducer and activator of transcription-3 signaling within the arcuate nucleus (ARC) in lean rats. Amylin (50 μg/kg · d) or leptin (125 μg/kg · d) infusion to lean rats decreased 28-d food intake (14 and 10%, respectively), body weight (amylin by 4.3%, leptin by 4.9%), and epididymal fat (amylin by 19%, leptin by 37%). Amylin/leptin co-infusion additively decreased food intake (by 26%) and reduced body weight (by 15%) and epididymal fat (by 78%; all P &lt; 0.05 vs. all groups) in a greater than mathematically additive manner, consistent with synergy. Amylin increased leptin binding within the ventromedial hypothalamus (VMN) by 35% and dorsomedial hypothalamus by 47% (both P &lt; 0.05 vs. vehicle). Amylin/leptin similarly increased leptin binding in the VMN by 40% and ARC by 70% (P &lt; 0.05 vs. vehicle). In amylin-deficient mice, hypothalamic leptin receptor mRNA expression was reduced by 50%, leptin-stimulated phosphorylated signal transducer and activator of transcription-3 within ARC and VMN was reduced by 40%, and responsiveness to leptin’s (1 mg/kg · d for 28 d) weight-reducing effects was attenuated (all P &lt; 0.05 vs. wild-type controls). We suggest that amylin/leptin’s marked weight- and fat-reducing effects are due to activation of intrinsic synergistic neuronal signaling pathways and further point to the integrated neurohormonal therapeutic potential of amylin/leptin agonism in obesity.

scholarly journals CNS β3-adrenergic receptor activation regulates feeding behavior, white fat browning, and body weight

2017 ◽  
Vol 313 (3) ◽  
pp. E344-E358 ◽  
Author(s):  
Jennifer E. Richard ◽  
Lorena López-Ferreras ◽  
Belén Chanclón ◽  
Kim Eerola ◽  
Peter Micallef ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Insulin Release ◽  
Adrenergic Receptor ◽  
Metabolic Regulation ◽  
Receptor Activation ◽  
Reduced Body ◽  
The Central Nervous System ◽  
The Brain

Pharmacological β3-adrenergic receptor (β3AR) activation leads to increased mitochondrial biogenesis and activity in white adipose tissue (WAT), a process commonly referred to as “browning”, and transiently increased insulin release. These effects are associated with improved metabolic function and weight loss. It is assumed that this impact of β3AR agonists is mediated solely through activation of β3ARs in adipose tissue. However, β3ARs are also found in the brain, in areas such as the brain stem and the hypothalamus, which provide multisynaptic innervation to brown and white adipose depots. Thus, contrary to the current adipocentric view, the central nervous system (CNS) may also have the ability to regulate energy balance and metabolism through actions on central β3ARs. Therefore, this study aimed to elucidate whether CNS β3ARs can regulate browning of WAT and other aspects of metabolic regulation, such as food intake control and insulin release. We found that acute central injection of β3AR agonist potently reduced food intake, body weight, and increased hypothalamic neuronal activity in rats. Acute central β3AR stimulation was also accompanied by a transient increase in circulating insulin levels. Moreover, subchronic central β3AR agonist treatment led to a browning response in both inguinal (IWAT) and gonadal WAT (GWAT), along with reduced GWAT and increased BAT mass. In high-fat, high-sugar-fed rats, subchronic central β3AR stimulation reduced body weight, chow, lard, and sucrose water intake, in addition to increasing browning of IWAT and GWAT. Collectively, our results identify the brain as a new site of action for the anorexic and browning impact of β3AR activation.

scholarly journals NEURONAL FGF-21 SIGNALING: A SENSOR OF DIETARY PROTEIN

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S730-S730
Author(s):  
Cristal Hill ◽  
Christopher Morrison
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Glucose Homeostasis ◽  
Dietary Protein ◽  
Protein Restriction ◽  
Fibroblast Growth Factor 21 ◽  
Dietary Protein Restriction ◽  
Reduced Body ◽  
Low Protein ◽  
The Central Nervous System

Abstract Our data demonstrates that dietary protein restriction increases energy expenditure and improves glucose homeostasis, and that this effect is largely mediated by the metabolic hormone fibroblast growth factor 21(FGF21). Considering that the central nervous system (CNS) is acknowledged as a major regulator of both energy and glucose homeostasis, we have extended our studies to identify the tissue site mediating these FGF21-dependent effects via dietary protein restriction. In this study, mice with dysfunctional FGF21-signaling in either the CNS or adipose tissue were fed a control or low protein (LP)-diet to assess changes in body weight and metabolic endpoints. Our data show that LP diet increased energy expenditure and reduced body weight in control littermates, but these effects were lost in mice bearing CNS-specific deletion of Klb. These data highlight a liver to brain FGF21-signal as the first known neuroendocrine mechanism to explain the coordinated metabolic changes induced by dietary protein restriction.

Effect of [Asu,]eel calcitonin on prolactin release in normal subjects and patients with prolactinoma

1985 ◽  
Vol 108 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Hidesuke Kaji ◽  
Kazuo Chihara ◽  
Naoto Minamitani ◽  
Hitoshi Kodama ◽  
Tetsuya Kita ◽  
...  
Keyword(s):  
Body Weight ◽  
Bolus Injection ◽  
Normal Subjects ◽  
Regular Insulin ◽  
Prolactin Release ◽  
Saline Administration ◽  
The Central Nervous System ◽  
Plasma Prl ◽  
Male Subjects

Abstract. The effect of [Asu]eel calcitonin (ECT), an equipotent analogue of eel CT, on prolactin (Prl) secretion was examined in 12 healthy male subjects and in 6 patients with prolactinoma. In healthy subjects, ECT (0.5 μg/kg body weight · h) or saline was infused for 2 h and TRH was injected iv as a bolus of 500 μg at 1 h of ECT or saline administration. ECT did not affect basal Prl levels during 1 h of infusion. TRH caused a significant increase of plasma Prl with peak values of 75.2 ± 11.6 ng/ml in ECT-infused subjects, which did not differ from those infused with saline (68.5 ± 8.3 ng/ml). Next, an iv bolus injection of regular insulin (0.1 U/kg body weight) was followed by an infusion of ECT or saline alone. Plasma Prl peaks after hypoglycaemic stress were significantly lower in ECT-infused subjects than those in saline-injected controls (ECT, 16.5 ± 3.1 vs 33.5 ± 9.6 ng/ml, P < 0.05). In patients with prolactinoma, basal levels of plasma Prl ranging from 42.0–4130 ng/ml failed to change during iv infusion of ECT. Moreover, ECT (10−9–10−6m) did not affect Prl release from prolactinoma tissues perifused in vitro. These findings suggest that ECT may not act directly on the pituitary to modify Prl release. Rather, peripherally administered ECT appears to suppress Prl release via the central nervous system.

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