Discover and read the best of Twitter Threads about #triglycerides
Most recents (24)
Here, a triple agonist that interacts with GLP-1, neuropeptide Y1&Y2 receptors, regulated insulin secretion in rat and human pancreatic islets, promoted insulin-independent Y1-R-mediated glucose uptake in rat muscle tissue ex vivo and reduced food intake and body weight in rats. 
- Mechanisms underlying long-term sustained weight loss and glycemic normalization after obesity surgery include changes in gut hormone levels, including glucagon-like peptide 1 (GLP-1) and peptide YY (PYY).
- PYY1–36 is a gut hormone that binds to the Y1-R in pancreatic islets and central nervous system nuclei that control appetite regulation in the brain including the brainstem area postrema and nucleus tractus solitarius, where it has an orexigenic effect.
The findings of this study suggest that inflammation (glycated proteins and small:total HDL particle ratio) and muscle metabolism (creatinine, creatine) may play a substantial role in the development of type 2 diabetes.
- The aim of this study was to combine nuclear magnetic resonance-based metabolomics and machine learning to find a glucose-independent molecular signature associated with future type 2 diabetes mellitus development.
- A case-control design nested in a population-based cohort (Di@bet.es study) was used in this study.
In this one, a higher cardiovascular risk, as assessed by the Framingham 10‐year cardiovascular disease risk score, was associated with poorer cognitive function among older adults living in the US.
- The Framingham 10‐year cardiovascular disease risk score is based on age, sex, smoking, total cholesterol, high‐density lipoprotein‐cholesterol, blood pressure, and diabetes.
- It was found to be associated with lower cognitive function among older adults, including overall cognition and particular domains of cognition, such as executive function and processing speed, and immediate and delayed memory.
In this one in patients with acute coronary syndrome, reductions in LDL particle electronegativity were linked to alterations of the LDL lipidome, and were associated with all-cause and cardiovascular mortality beyond some established risk factors during a 1-year follow-up.
"In a prospective cohort of contemporary patients with ACS, we demonstrate for the first time that attenuated LDL electronegativity, as assessed by the L1-L5 ratio...
"...unfavorably associates with all-cause and cardiovascular mortality after the index ACS, over and above the updated GRACE risk score...
The findings of this one suggest a possible defect in the transfer of PUFA from peripheral tissues to the liver in NAFLD, with HDL composition being tightly connected to the rewiring of hepatic PUFA composition that occurs in NAFLD.
- NAFLD was characterised by a depletion in phospholipids (phosphatidylcholines, phosphatidylethanolamines, phosphatidylglycerols and sphingomyelins) specifically driven by their PUFA fraction.
- NAFLD patients had higher saturated and lower polyunsaturated FFAs.
The findings of this one suggest that the glycaemic load of a meal is not a major determinant of postprandial response, with a greater impact exerted by the metabolic health of the individual.
- The aim of this study was to perform an acute cross-over intervention to examine the interactive actions of meal glycaemic load on the dynamic responses of the plasma metabolome in overweight females.
- Postmenopausal women with a mean age of 63 yeras ingested two differing high-carbohydrate test meals (73 g carbohydrate; 51% energy) composed of either low glycemic index or high glycemic index foods in a randomised sequence.
This one suggests that low circulating adiponectin is a key damaging element for β-cells.
- Diluted plasma from human donors with obesity acutely impaired β-cell integrity and insulin secretion relative to plasma from lean subjects.
- Similar results were observed with diluted sera from obese rats fed ad libitum, when compared to sera from lean, calorically restricted, animals.
In this one, NAFLD, as assessed by the fatty liver index (FLI), was found associated with the risk of type 2 diabetes in Japanese adults.
* LP (linear predictor) = 0.953*ln[triglycerides (mg/dL)] + 0.139 * BMI (kg/m2) + 0.718*ln[GGT (IU/L)] + 0.053 * waist circumference (cm) - 15.745
* FLI = [e^LP/(1 + e^LP)] * 100
* FLI = [e^LP/(1 + e^LP)] * 100
- The FLI was positively associated with the risk of type 2 diabetes.
Interestingly, using NMR spectroscopy, this one suggests that newly manifest type 2 diabetes-associated dyslipoproteinemia does not significantly change the total concentrations of the lipoproteins produced in the liver, but selectively their subclass distributions.
- In the present study, German long time blood donors that were assumed to be healthy according to the rules applying for blood donors were examined.
Impaired fasting glucose, impaired glucose tolerance or manifest type 2 diabetes were not known for this group before they were included in this study.
Contrary to other studies, in this Spanish population with high cardiovascular risk, higher cardiovascular health score using the American Heart Association's Life’s Simple 7 metrics was associated with a decreased risk of incident atrial fibrillation in lean individuals only.
- The American Heart Association’s Life’s Simple 7 health score consists of 7 modifiable metrics: physical activity, diet, smoking status, BMI, systolic blood pressure, fasting plasma glucose, and cholesterol.
This one discovered three discrete hyperuricemia trajectories over a 5-year span and found that those in the hyperuricemia high-increasing pattern, as compared with those in the low-stable pattern, were at an increased risk of diabetes.
- According to the characteristics of their hyperuricemia status changes during this 5-year exposure period, subjects were divided into three different hyperuricemia trajectory groups:
The “low-stable” trajectory, the “moderate-stable” trajectory and the “high-increasing” trajectory.
The findings of this one suggest that persistent de novo lipogenesis during fasting may at least partly explain impaired fasting ketogenesis in metabolic syndrome, which appears to be the consequence of reciprocal regulation of DNL and β-oxidation.
- Forty non-diabetic individuals with and without a history of NAFL were recruited for this study.
- Lipogenesis remained detectable in a subset of individuals after a 24 hour fast, including some subjects without hepatic steatosis or other hallmarks of metabolic syndrome.
In this one, adipsin, an adipokine that can stimulate triglyceride synthesis and is involved in the complement system, was found to be associated with MAFLD.
- Individuals with MAFLD had higher levels of adipsin.
- In indivisuals with MAFLD, as the number of metabolic risk abnormalities increased, the levels of serum adipsin and the proportion of moderate to severe fatty liver disease also increased.
Here, both metabolically healthy and metabolically unhealthy obesity were associated with higher risk of cancer, although though the risk relationships were weaker in the latter case.
- The combination of obesity and metabolically unhealthy status conveyed the highest risk of any obesity-related cancer, compared to other combinations of BMI and metabolic health status.
- The increased risk was found for most obesity-related cancers, with the highest relative risks found for endometrial, liver, and renal cell cancer.
This one delves further into the cardiometabolic impact of body fat distribution, finding associations between visceral, abdominal subcutaneous, and gluteofemoral adipose tissue volumes at scale and risk of type 2 diabetes, and coronary artery disease.
This is not the first study of this group in this subject. They have done some previous, related, and very interesting work on the matter:
- The intention was to quantify visceral, abdominal subcutaneous, and gluteofemoral adipose tissue volumes at scale using machine learning and data from the studies mentioned above, in order to determine associations with type 2 diabetes and coronary artery disease.
Here, total intakes of folate, vitamin B6, and vitamin B12 were inversely associated with the incidence of meatbolic syndrome and the majority of its individual components among adults in the US.
- Folate intake was inversely associated with all of the individual components of the metabolic syndrome.
- The inverse association between vitamin B6 and metabolic syndrome appeared to be mainly explained by its favorable outcomes on adiposity, hypertriglyceridemia, low HDL-C, and elevated blood pressure.
This one found that the association between obesity and cardiovascular disease is mediated by the triglyceride glucose (TyG) index, a surrogate marker of insulin resistance.
- TyG index: ln (fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2).
- The proportion mediated was 47.81% for overweight, 37.94% for general obesity and 32.01%, 35.02%, and 31.06% for central obesity measured by waist circumference, waist-to-hip ratio, and waist-to-height ratio, respectively.
🧵 Dec 9th anniversary thread
On this day in 2015 I received a lab result that would alter the course of my life.
Just two weeks earlier I had gotten my very first bloodwork after half a year on #keto that showed my total and #LDL #Cholesterol had nearly doubled (!)… /1
On this day in 2015 I received a lab result that would alter the course of my life.
Just two weeks earlier I had gotten my very first bloodwork after half a year on #keto that showed my total and #LDL #Cholesterol had nearly doubled (!)… /1
2/ With that first test I was overcome with shock and curiosity — much more former than the latter.
I wanted to get a repeat test to confirm this wasn’t a lab error.
I wasn’t ready to give up #keto, but I was miserable enough that I ate considerably less.
I wanted to get a repeat test to confirm this wasn’t a lab error.
I wasn’t ready to give up #keto, but I was miserable enough that I ate considerably less.
3/ At the same time I learned as much as I could about Lipidology - which focuses on how the body moves lipids (like cholesterol) in the blood.
And to my surprise, this system is already very familiar to me as a software engineer given it is a distributed object network.
And to my surprise, this system is already very familiar to me as a software engineer given it is a distributed object network.
🧵1/8 Here's an easy thread for reference on our current papers. 👇👇👇
🔖 Bookmark this!
We cover:
- High #LDL on #lowcarb/#keto
- Lean Mass Hyper-responders (#LMHR)
- The Lipid Energy Model (#LEM)
- And, ofc, our #LMHRstudy underway right now
🔖 Bookmark this!
We cover:
- High #LDL on #lowcarb/#keto
- Lean Mass Hyper-responders (#LMHR)
- The Lipid Energy Model (#LEM)
- And, ofc, our #LMHRstudy underway right now
2/8 The #LMHRpaper was our first describing the #LMHR phenotype
- #LDL #Cholesterol of 200 or higher
- #HDL #Cholesterol of 80 mg or higher
and
- #Triglycerides of 70 mg or lower
Which is actually common for lean, very folks on #lowcarb/#keto folks. doi.org/10.1093/cdn/nz…
- #LDL #Cholesterol of 200 or higher
- #HDL #Cholesterol of 80 mg or higher
and
- #Triglycerides of 70 mg or lower
Which is actually common for lean, very folks on #lowcarb/#keto folks. doi.org/10.1093/cdn/nz…
3/8 Our second paper brings a case report on a single #LMHR with extremely high #LDLc (~500 mg/dL) for 2.5 years, their eating patterns, and current CT angiography.
(⚠️Please note this is a single case report and should be considered anecdotal, ofc) doi.org/10.3389/fendo.…
(⚠️Please note this is a single case report and should be considered anecdotal, ofc) doi.org/10.3389/fendo.…
1/ Alright, let's chat the #NHANES (IV)
As usual, I'll give my caveats this is back-of-the-envelope on data I wrangled via CDC on this expansive dataset -- and it's associational, ofc (observational)
So what are the lipids like for those who live to 100yr in NHANES?
As usual, I'll give my caveats this is back-of-the-envelope on data I wrangled via CDC on this expansive dataset -- and it's associational, ofc (observational)
So what are the lipids like for those who live to 100yr in NHANES?
2/ Remember, these aren't the lipid levels taken *at* age 100+, it's what their levels where at the time of examination 15-20 years prior.
This is very relevant when considering reverse causality given this extreme gap in time for all who were reaching centenarian status.
This is very relevant when considering reverse causality given this extreme gap in time for all who were reaching centenarian status.
3/ First up -- #LDL #Cholesterol.
Yes, 73% of you correctly guessed 130mg/dL is the mean average for these 32 individuals (lipids taken age 85 or earlier).
LDL mean average: 130 mg/dL
0% 25% 50% 75% 100%
72.0 102.5 126.0 154.0 215.0
Yes, 73% of you correctly guessed 130mg/dL is the mean average for these 32 individuals (lipids taken age 85 or earlier).
LDL mean average: 130 mg/dL
0% 25% 50% 75% 100%
72.0 102.5 126.0 154.0 215.0
This systematic review and meta-analysis suggests that CoQ10 supplementation is likely to improve lipid profiles in adults, with the optimal dose being 400-500mg/day.
- CoQ10 supplementation is likely to decrease total cholesterol, LDL-c, and TG and increase HDL-c levels in the adult population.
- Dose–response analysis revealed an inverse J-shaped nonlinear pattern between CoQ10 supplementation and TC, in which the optimal dose was 400 to 500 mg/day.
In this one, mice fed an obesogenic high starch diet, although exhibited hyperglycemia and hyperinsulinemia, remained glucose tolerant and insulin sensitive despite having excess adipose tissue, in contrast to mice fed an obesogenic high-fat diet.
This is a pretty cool study delving further into the connection between ceramides, de novo lipogenesis and liver, muscle fat infiltration, the relationship between body fat content and insulin action and the effects of dietary manipulation in these factors.
- The current study reports on a dietary intervention that produces significant obesity but maintains normal insulin action in mice providing some mechanistic understanding of the phenomenon of obesity with preserved insulin sensitivity.
Now that's interesting.
This one in mice suggests that chronic glucagon agonist-mediated weight loss is due to low plasma amino acid availability, which results in increased energy expenditure and subsequent body weight loss.
This one in mice suggests that chronic glucagon agonist-mediated weight loss is due to low plasma amino acid availability, which results in increased energy expenditure and subsequent body weight loss.
- A long-acting glucagon analog led to glucagon-mediated body weight loss which was intrinsically linked to hypoaminoacidemia.
- Low plasma amino acids were found to be a pre-requisite for this glucagon-mediated energy expenditure and weight loss.
🧵 New paper on comparing advanced lipid testing (NMR) with body fat (adiposity) - ht @nicknorwitz
High adiposity associates with:
- ⬆️ #ApoB & #LDL-C
- ⬆️ #triglycerides
- ⬆️ levels of all fatty acids
How does this relate to #LEM? Let's unpack... /1
nature.com/articles/s4385…
High adiposity associates with:
- ⬆️ #ApoB & #LDL-C
- ⬆️ #triglycerides
- ⬆️ levels of all fatty acids
How does this relate to #LEM? Let's unpack... /1
nature.com/articles/s4385…
2/ "Adiposity-related hypertriglyceridemia is mainly driven by increased numbers of triglyceride-rich VLDLs (which carry the largest proportion of triglycerides in blood). Concurrently, the cholesterol in these lipoproteins also seem to be higher at higher adiposity levels."
3/ And these next sentences are key -- take special note of the underlined text...
