Tuesday, March 4, 2014

Can Eating More Fat Make You Leaner?

sharma-obesity-visceral-fat-mriYes, if the excess fat is poly-unsaturated – no, if it is saturated.

At least this was the finding in an overfeeding study conducted by Fredrik Rosqvist and colleagues from the Uppsala University, Sweden, published in DIABETES.

The study with the memorable acronym LIPOGAIN, was a double-blind, parallel-group, randomized trial involving 39 young normal-weight individuals who were overfed muffins either high in saturated fats (palm oil) or in n-6 poly-unsaturated fats (sunflower oil) for seven weeks.

The number of muffins that each subject had to consume were individually adjusted to ensure that each subject increased their body weight by about 1.5 Kg (or 3%). To achieve this, the subjects consumed on average three muffins or about an extra 750 kcals/day.

However, where the excess calories went was quite different.

While the subjects eating saturated fat markedly increased their liver fat and gained almost twice as much visceral fat as those in the poly-unsaturated fat group, the latter experienced a nearly three-fold larger increase in lean tissue than the saturated fat group.

The two diets also had quite different effects on the expression of genes regulating energy dissipation, insulin resistance, body composition and fat cell differentiation in subcutaneous fat tissue.

Thus, the authors conclude that while overeating saturated fat promotes liver and visceral fat storage, the excess energy from poly-unsaturated fat may instead promote the growth of lean tissue.

What I learnt from this study is that there are indeed important differences in how the body handles excess calories depending on where they come from.

In that respect at least, not all calories are equal.

Edmonton, AB

Fat Jokes Are Not Funny! Help publish this anti-bullying children’s book

ResearchBlogging.orgRosqvist F, Iggman D, Kullberg J, Jonathan Cedernaes J, Johansson HE, Larsson A, Johansson L, Ahlström H, Arner P, Dahlman I, & Risérus U (2014). Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans. Diabetes PMID: 24550191


VN:F [1.9.22_1171]
Rating: 10.0/10 (1 vote cast)
VN:F [1.9.22_1171]
Rating: +1 (from 1 vote)

Monday, November 18, 2013

Harnessing Brown Adipose Tissue to Fight Obesity?

Brown Fat Cells in White Fat Tissue

Brown Fat Cells in White Fat Tissue

Although obesity is largely a “calories-in” rather than a “calories-out” problem, emerging evidence points to the possibilities of harnessing thermogenic brown adipose tissue to help balance this equation by helping burn more calories.

But this may be more difficult than it sounds.

Readers interested in this issue, may wish to refer to an overview of this topic by Canadian Obesity Network Bootcamper Kanta Chachi and colleagues from the University of Montreal, published in Obesity Reviews.

The paper summarizes talks given by various experts in the field at the 11th Stock Conference in Montreal, October 2012.

This includes an analysis of our current understanding of the developmental origin, cellular properties and molecular distinctions between classical brown and beige/brite adipocytes as well as the central circuitries and neuropeptides involved in the regulation of brown adipocyte thermogenesis.

The presence and metabolic activity of brown adipose tissue and its role in various aspects of human energy metabolism, including diet-induced thermogenesis is also discussed.

As for the potential therapeutic utility of brown adipocytes for treating obesity in humans, it is important to distinguish between t BAT mass and BAT activity – thus therapeutic approaches could focus on either increasing the amount of BAT present or increasing the activity of tissue that is already present.

As the authors point out,

“Even if there is no doubt that BAT can be activated by behavioural or pharmacological means, it is doubtful that BAT activation will be a viable strategy for weight loss. Based on the recent studies reporting enhanced energy expenditure in humans upon stimulation of BAT thermogenesis, it is conceivable that activation of BAT may rather be developed as a strategy for maintenance of weight loss achieved by other therapies. Indeed, BAT activation would counteract the ‘metabolic adaptation’ occurring in response to weight loss.”


“Considering that energy balance is a tightly regulated phenomenon, it is likely that BAT-mediated increase in energy expenditure may activate metabolic adaptations or counter-regulatory mechanisms in the body, which could oppose weight loss, in a similar fashion to what is seen with caloric restriction- or exercise-induced weight loss programmes.


“Whether BAT-mediated weight loss would promote similar metabolic adaptations and counter-regulatory mechanisms – including an increase in food intake remain to be determined. Although BAT thermogenesis is an attractive candidate, we are still in the preliminary stages of utilizing this tissue as a therapy for obesity. It would be important to practice ‘caution in extrapolating indirect histological and thermographic evidence to a major role for BAT in human energy metabolism’”

Edmonton, AB

ResearchBlogging.orgChechi K, Nedergaard J, & Richard D (2013). Brown adipose tissue as an anti-obesity tissue in humans. Obesity reviews : an official journal of the International Association for the Study of Obesity PMID: 24165204



VN:F [1.9.22_1171]
Rating: 10.0/10 (2 votes cast)
VN:F [1.9.22_1171]
Rating: +2 (from 2 votes)

Sunday, October 20, 2013

Obesity Weekend Roundup, October 18, 2013

As not everyone may have a chance during the week to read every post, here’s a roundup of last week’s posts:

Have a great Sunday! (or what is left of it)

Edmonton, AB

VN:F [1.9.22_1171]
Rating: 0.0/10 (0 votes cast)
VN:F [1.9.22_1171]
Rating: 0 (from 0 votes)

Friday, October 18, 2013

Is Obesity a Cardiovascular Risk Factor?

sharma-obesity-cardiac-rehabThis morning I am presenting a plenary talk for the Canadian Association of Cardiac Rehabilitation at the Vascular 2013 conference in Montreal.

This topic is certainly relevant to this organisation, as, in a paper published in the Journal of Cardiopulmonary Rehabilitation back in 2004, we showed that about 35% of patients seen in cardiac rehab programs have a BMI greater than 30 kg/m2.

Thus, it was not surprising that the topic I was asked to speak on, is whether or not obesity is a cardiovascular risk factor.

As I hopefully made clear in my presentation, this is not as straightforward a question as many may think.

No doubt, excess body fat is associated with well-known risk factors for cardiovascular disease including hypertension, dyslipidemia and diabetes mellitus.

However, we have also learnt that much depends on the molecular and cellular composition as well as the anatomical location of this excess fat.

While intra-abdominal or visceral fat as well as other ectopic fat depots (e.g. heart, muscle, liver) are strongly associated with cardiovascular risk factors, excess fat deposition limited to subcutaneous depots (particularly hips and thighs) may even be deemed protective.

Thus, whether or not excess body fat is a risk factor for cardiovascular problems really depends on the exact nature of that fat.

That said, there are other aspects of excess weight that warrant medical attention.

Although, diabetes may be the most important predictor of mortality in obese individuals (see yesterday’s post), there are other significant health problems associated with excess weight (arthritis, sleep apnea, reflux disease, urinary incontinence, etc.) that may exist even in the otherwise metabolically healthy obese individuals.

As we showed in our 2004 paper, substantial benefits on cardiovascular risk factors can be derived from exercise-based cardiac rehab programs even with minimal or no weight loss.

Whether or not weight loss significantly adds to reducing cardiovascular risk in the long-term, interestingly enough, still needs to be demonstrated.

Montreal, QC



VN:F [1.9.22_1171]
Rating: 10.0/10 (2 votes cast)
VN:F [1.9.22_1171]
Rating: +1 (from 1 vote)

Wednesday, January 2, 2013

Mitochondrial Protein Makes You Healthy and Fat

While some readers may be hoping for the latest diet breakthrough, researchers have now discovered an even easier way to get those calories straight from your lips to your hips.

Thus, according to a paper from Phil Scherer’s lab published in Nature Medicine, the secret ingredient is an unassuming protein that lives in your mitochondria (those crinkly looking cellular powerhouses that run your energy metabolism).

As the story goes, this protein, with the rather memorable name MitoNEET, allows your fat cells to gobble up even more fat, thereby keeping it from ruining the neighbourhood in other organs (like your liver or skeletal muscle).

Evidently, MitoNEET messes up mitochondrial iron transport thereby reducing fat-burn (ß-oxidation), which also leaves you with fewer pro-inflammatory oxygen radicals and more metabolically friendly adiponectin floating around.

So, while an extra dose of MitoNEET may well make you fatter, you can rejoice in the knowledge that this fat is safely tucked away where it belongs, namely in your white fat – point being, it no longer messes with your glucose levels or clogs up your arteries – or at least this is how the story goes if you happen to be a lab mouse.

And woe to those, who lack this fat-enriching protein – they become skinny and unhealthy beings on a down-hill path to certain diabetes, heart disease, and male-pattern baldness (I made up that last one, but it’s probably true).

While anti-obesity activists may wonder about the usefulness of this research, I can certainly see a hot emerging market for MitoNEET analogues in places where beauty is measured in (extra) pounds (like Barbados).

And, if you happen to be one of those healthy obese (EOSS Stage 0) folk, it’s perhaps high time you added MitoNEET to your list of blessings.

Edmonton, Alberta
Kusminski CM, Holland WL, Sun K, Park J, Spurgin SB, Lin Y, Askew GR, Simcox JA, McClain DA, Li C, & Scherer PE (2012). MitoNEET-driven alterations in adipocyte mitochondrial activity reveal a crucial adaptive process that preserves insulin sensitivity in obesity. Nature medicine, 18 (10), 1539-49 PMID: 22961109

VN:F [1.9.22_1171]
Rating: 10.0/10 (3 votes cast)
VN:F [1.9.22_1171]
Rating: +1 (from 1 vote)

In The News

Diabetics in most need of bariatric surgery, university study finds

Oct. 18, 2013 – Ottawa Citizen: "Encouraging more men to consider bariatric surgery is also important, since it's the best treatment and can stop diabetic patients from needing insulin, said Dr. Arya Sharma, chair in obesity research and management at the University of Alberta." Read article

» More news articles...


"Metabolically healthy overweight and obesity."

» Browse and download more journal publications...

Watch Dr. Sharma in the News!

Dr. Sharma - NEWS Videos

Listen to Dr. Sharma!

Dr. Sharma - on CBC.ca

Watch Dr. Sharma on Listen Up

  • Subscribe via Email

    Enter your email address:

    Delivered by FeedBurner

  • Arya Mitra Sharma
  • Disclaimer

    Postings on this blog represent the personal views of Dr. Arya M. Sharma. They are not representative of or endorsed by Alberta Health Services or the Weight Wise Program.
  • Archives


  • RSS Weighty Matters

  • Click for related posts

  • Disclaimer

    Medical information and privacy
    Any medical discussion on this page is intended to be of a general nature only. This page is not designed to give specific medical advice. If you have a medical problem you should consult your own physician for advice specific to your own situation.

  • Meta

  • Obesity Links

  • If you have benefitted from the information on this site, please take a minute to donate to its maintenance.

  • Home | News | KOL | Media | Publications | Trainees | About
    Copyright 2008–2014 Dr. Arya Sharma, All rights reserved.
    Blog Widget by LinkWithin