scholarly journals Amylin and Calcitonin: Potential Therapeutic Strategies to Reduce Body Weight and Liver Fat

2021 ◽  
Vol 11 ◽  
Author(s):  
David S. Mathiesen ◽  
Asger Lund ◽  
Tina Vilsbøll ◽  
Filip K. Knop ◽  
Jonatan I. Bagger
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Gastric Emptying ◽  
Pancreatic Beta Cells ◽  
Metabolic Diseases ◽  
Body Weight Loss ◽  
Liver Fat ◽  
Metabolic Effects ◽  
Human Organism ◽  
Alcoholic Fatty Liver

The hormones amylin and calcitonin interact with receptors within the same family to exert their effects on the human organism. Calcitonin, derived from thyroid C cells, is known for its inhibitory effect on osteoclasts. Calcitonin of mammalian origin promotes insulin sensitivity, while the more potent calcitonin extracted from salmon additionally inhibits gastric emptying, promotes gallbladder relaxation, increases energy expenditure and induces satiety as well as weight loss. Amylin, derived from pancreatic beta cells, regulates plasma glucose by delaying gastric emptying after meal ingestion, and modulates glucagon secretion and central satiety signals in the brain. Thus, both hormones seem to have metabolic effects of relevance in the context of non-alcoholic fatty liver disease (NAFLD) and other metabolic diseases. In rats, studies with dual amylin and calcitonin receptor agonists have demonstrated robust body weight loss, improved glucose tolerance and a decreased deposition of fat in liver tissue beyond what is observed after a body weight loss. The translational aspects of these preclinical data currently remain unknown. Here, we describe the physiology, pathophysiology, and pharmacological effects of amylin and calcitonin and review preclinical and clinical findings alluding to the future potential of amylin and calcitonin-based drugs for the treatment of obesity and NAFLD.

Characterization of one anastomosis gastric bypass and impact of biliary and common limbs on bile acid and postprandial glucose metabolism in a minipig model

2021 ◽  
Author(s):  
Camille Marciniak ◽  
Oscar Chávez-Talavera ◽  
Robert Caiazzo ◽  
Thomas Hubert ◽  
Lorea Zubiaga ◽  
...  
Keyword(s):  
Weight Loss ◽  
Gastric Bypass ◽  
Body Weight ◽  
Glucose Metabolism ◽  
Glucose Homeostasis ◽  
Body Weight Loss ◽  
Metabolic Effects ◽  
One Anastomosis Gastric Bypass ◽  
Alimentary Limb ◽  
The Common

Background/Objectives: The alimentary limb has been proposed to be a key driver of the weight-loss-independent metabolic improvements that occur upon bariatric surgery. However, the One Anastomosis Gastric Bypass (OAGB) procedure, consisting of one long biliary limb and a short common limb, induces stronger beneficial metabolic effects compared to Roux-en-Y Gastric Bypass (RYGB) in humans, despite the lack of an alimentary limb. The aim of this study was to assess the role of the biliary and common limbs in the weight-loss and metabolic effects that occur upon OAGB. Subjects/Methods: OAGB and sham surgery, with or without modifications of the length of either the biliary limb or the common limb, were performed in Gottingen-like minipigs. Weight loss, metabolic changes, and the effects on plasma and intestinal bile acids (BAs) were assessed 15 days after surgery. Results: OAGB significantly decreased body weight, improved glucose homeostasis, increased postprandial GLP-1 and fasting plasma BAs, and qualitatively changed the intestinal BA species composition. Resection of the biliary limb prevented the body weight loss effects of OAGB and attenuated the postprandial GLP-1 increase. Improvements in glucose homeostasis along with changes in plasma and intestinal BAs occurred after OAGB regardless of the biliary limb length. Resection of only the common limb reproduced the glucose homeostasis effects and the changes in intestinal BAs. Conclusions: Our results suggest that the changes in glucose metabolism and BAs after OAGB are mainly mediated by the length of the common limb, whereas the length of the biliary limb contributes to body weight loss.

scholarly journals Beyond Body Weight-Loss: Dietary Strategies Targeting Intrahepatic Fat in NAFLD

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1316 ◽  
Author(s):  
Nicolai Worm
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Body Weight ◽  
Liver Disease ◽  
Glycogen Synthesis ◽  
Liver Fat ◽  
Meal Replacement ◽  
Alcoholic Fatty Liver ◽  
Therapeutic Concept ◽  
The Metabolic Syndrome

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent liver disease in industrialized countries. It is regarded as the hepatic manifestation of the metabolic syndrome (MetS) resulting from insulin resistance. Moreover, insulin resistance impairs glycogen synthesis, postprandially diverting a substantial amount of carbohydrates to the liver and storing them there as fat. NAFLD has far-reaching metabolic consequences involving glucose and lipoprotein metabolism disorders and risk of cardiovascular disease, the leading cause of death worldwide. No pharmaceutical options are currently approved for the treatment of NAFLD. Exercise training and dietary interventions remain the cornerstone of NAFLD treatment. Current international guidelines state that the primary goal of nutritional therapy is to reduce energy intake to achieve a 7%–10% reduction in body weight. Meal replacement therapy (formula diets) results in more pronounced weight loss compared to conventional calorie-restricted diets. However, studies have shown that body mass index (BMI) or weight reduction is not obligatory for decreasing hepatic fat content or to restore normal liver function. Recent studies have achieved significant reductions in liver fat with eucaloric diets and without weight loss through macronutrient modifications. Based on this evidence, an integrative nutritional therapeutic concept was formulated that combines the most effective nutrition approaches termed “liver-fasting.” It involves the temporary use of a low calorie diet (total meal replacement with a specific high-protein, high-soluble fiber, lower-carbohydrate formula), followed by stepwise food reintroduction that implements a Mediterranean style low-carb diet as basic nutrition.

scholarly journals Similar Weight Loss Induces Greater Improvements in Insulin Sensitivity and Liver Function among Individuals with NAFLD Compared to Individuals without NAFLD

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 544 ◽  
Author(s):  
Ruth Schübel ◽  
Tobias Nonnenmacher ◽  
Disorn Sookthai ◽  
Sandra Gonzalez Maldonado ◽  
Solomon Sowah ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Liver Function ◽  
Dietary Intervention ◽  
Fat Content ◽  
Metabolic Parameters ◽  
Liver Fat ◽  
Metabolic Effects ◽  
Liver Fat Content ◽  
Alcoholic Fatty Liver

Background: Preliminary evidence suggests that weight loss among obese has differential metabolic effects depending on the presence of non-alcoholic fatty liver disease (NAFLD). We assessed whether NAFLD predisposes to differential changes in liver fat content, liver function, and metabolic parameters upon diet-induced weight loss in a 50-week intervention trial. Methods: 143 overweight and obese non-smokers underwent a 12-week dietary intervention and a 38-week follow-up. Diet-induced changes in anthropometric measures, circulating biomarkers, and magnetic resonance (MR)-derived liver fat content and adipose tissue volumes were evaluated by mixed linear models stratifying by NAFLD at baseline. Results: The prevalence of NAFLD at baseline was 52%. Diet-induced weight loss after 12 (NAFLD: 4.8 ± 0.5%, No NAFLD: 5.1 ± 0.5%) and 50 weeks (NAFLD: 3.5 ± 0.7%, No NAFLD: 3.5 ± 0.9%) was similar in both groups, while the decrease in liver fat was significantly greater in the NAFLD group (week 12: 32.9 ± 9.5% vs. 6.3 ± 4.0%; week 50: 23.3 ± 4.4% vs. 5.0 ± 4.2%). Decreases in biomarkers of liver dysfunction (GGT, ALT, AST) and HOMA IR were also significantly greater in the NAFLD group. Other metabolic parameters showed no significant differences. Conclusion: Our data suggest that individuals with NAFLD show greater improvements of liver function and insulin sensitivity after moderate diet-induced weight loss than individuals without NAFLD.

scholarly journals Amylin-Mediated Restoration of Leptin Responsiveness in Diet-Induced Obesity: Magnitude and Mechanisms

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5679-5687 ◽  
Author(s):  
James L. Trevaskis ◽  
Todd Coffey ◽  
Rebecca Cole ◽  
Chunli Lei ◽  
Carrie Wittmer ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Combination Treatment ◽  
Body Weight Loss ◽  
Metabolic Effects ◽  
Fat Utilization ◽  
Diet Induced Obesity ◽  
Expression Of Genes ◽  
Obese Rats

Previously, we reported that combination treatment with rat amylin (100 μg/kg·d) and murine leptin (500 μg/kg·d) elicited greater inhibition of food intake and greater body weight loss in diet-induced obese rats than predicted by the sum of the monotherapy conditions, a finding consistent with amylin-induced restoration of leptin responsiveness. In the present study, a 3 × 4 factorial design was used to formally test for a synergistic interaction, using lower dose ranges of amylin (0, 10, and 50 μg/kg·d) and leptin (0, 5, 25, and 125 μg/kg·d), on food intake and body weight after 4 wk continuous infusion. Response surface methodology analysis revealed significant synergistic anorexigenic (P < 0.05) and body weight-lowering (P < 0.05) effects of amylin/leptin combination treatment, with up to 15% weight loss at doses considerably lower than previously reported. Pair-feeding (PF) experiments demonstrated that reduction of food intake was the predominant mechanism for amylin/leptin-mediated weight loss. However, fat loss was 2-fold greater in amylin/leptin-treated rats than PF controls. Furthermore, amylin/leptin-mediated weight loss was not accompanied by the counterregulatory decrease in energy expenditure and chronic shift toward carbohydrate (rather than fat) utilization observed with PF. Hepatic gene expression analyses revealed that 28 d treatment with amylin/leptin (but not PF) was associated with reduced expression of genes involved in hepatic lipogenesis (Scd1 and Fasn mRNA) and increased expression of genes involved in lipid utilization (Pck1 mRNA). We conclude that amylin/leptin interact synergistically to reduce body weight and adiposity in diet-induced obese rodents through a number of anorexigenic and metabolic effects.

1965-P: Glucagon Receptor Agonism Stimulates Body Weight Loss in Antibiotic Treatment in Obese Mice

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1965-P
Author(s):  
TEAYOUN KIM ◽  
JESSICA P. ANTIPENKO ◽  
SHELLY NASON ◽  
NATALIE PRESEDO ◽  
WILLIAM J. VAN DER POL ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Antibiotic Treatment ◽  
Body Weight Loss ◽  
Obese Mice ◽  
Glucagon Receptor

Relation between change in treatment for central diabetes insipidus and body weight loss

2018 ◽  
Vol 44 (1) ◽  
Author(s):  
Ayako Ito ◽  
Aya Nozaki ◽  
Ichiro Horie ◽  
Takao Ando ◽  
Atsushi Kawakami
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Diabetes Insipidus ◽  
Body Weight Loss ◽  
Central Diabetes Insipidus

scholarly journals Isoquinoline Alkaloids in Sows’ Diet Reduces Body Weight Loss during Lactation and Increases IgG in Colostrum

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2195
Author(s):  
Ester Arévalo Sureda ◽  
Xuemei Zhao ◽  
Valeria Artuso-Ponte ◽  
Sophie-Charlotte Wall ◽  
Bing Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Body Weight ◽  
Body Weight Loss ◽  
Muscle Thickness ◽  
Passive Immunity ◽  
Isoquinoline Alkaloids ◽  
Back Muscle ◽  
Fat Thickness ◽  
And Performance

Isoquinoline alkaloids (IQ) exert beneficial antimicrobial and anti-inflammatory effects in livestock. Therefore, we hypothesized that supplementing sows’ diets with IQ during gestation would decrease farrowing stress, affecting the piglets’ development and performance. Sows were divided into: IQ1, supplemented with IQ from gestation day 80 (G80) to weaning; IQ2, supplemented from gestation day 110 (G110) to weaning, and a non-supplemented (NC) group. Sow body weight (BW), feed intake, back-fat thickness and back-muscle thickness were monitored. Cortisol, glucose and insulin were measured in sows’ blood collected 5 d before, during, and after 7 d farrowing. Protein, fat, IgA and IgG were analyzed in the colostrum and milk. Piglets were monitored for weight and diarrhea score, and for ileum histology and gene expression 5 d post-weaning. IQ-supplemented sows lost less BW during lactation. Glucose and insulin levels were lower in the IQ groups compared to NC-sows 5 d before farrowing and had higher levels of protein and IgG in their colostrum. No other differences were observed in sows, nor in the measured parameters in piglets. In conclusion, IQ supplementation affected sows’ metabolism, reducing body weight loss during lactation. Providing IQ to sows from their entrance into the maternity barn might be sufficient to induce these effects. IQ improved colostrum quality, increasing the protein and IgG content, improving passive immunity for piglets.

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